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  • Cell Line  (202)
  • Models, Biological  (119)
  • Nature Publishing Group (NPG)  (313)
  • American Geophysical Union
  • Essen : Verl. Glückauf
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
  • Springer Nature
  • 2005-2009  (313)
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  • 1
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    Reprogramming towards pluripotency requires AID-dependent DNA demethylation (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-12-23
    Description: Reprogramming of somatic cell nuclei to yield induced pluripotent stem (iPS) cells makes possible derivation of patient-specific stem cells for regenerative medicine. However, iPS cell generation is asynchronous and slow (2-3 weeks), the frequency is low (〈0.1%), and DNA demethylation constitutes a bottleneck. To determine regulatory mechanisms involved in reprogramming, we generated interspecies heterokaryons (fused mouse embryonic stem (ES) cells and human fibroblasts) that induce reprogramming synchronously, frequently and fast. Here we show that reprogramming towards pluripotency in single heterokaryons is initiated without cell division or DNA replication, rapidly (1 day) and efficiently (70%). Short interfering RNA (siRNA)-mediated knockdown showed that activation-induced cytidine deaminase (AID, also known as AICDA) is required for promoter demethylation and induction of OCT4 (also known as POU5F1) and NANOG gene expression. AID protein bound silent methylated OCT4 and NANOG promoters in fibroblasts, but not active demethylated promoters in ES cells. These data provide new evidence that mammalian AID is required for active DNA demethylation and initiation of nuclear reprogramming towards pluripotency in human somatic cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2906123/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2906123/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhutani, Nidhi -- Brady, Jennifer J -- Damian, Mara -- Sacco, Alessandra -- Corbel, Stephane Y -- Blau, Helen M -- AG009521/AG/NIA NIH HHS/ -- AG024987/AG/NIA NIH HHS/ -- AI007328/AI/NIAID NIH HHS/ -- R01 AG009521/AG/NIA NIH HHS/ -- R01 AG009521-25/AG/NIA NIH HHS/ -- R01 AG024987/AG/NIA NIH HHS/ -- R01 AG024987-05/AG/NIA NIH HHS/ -- T32 AI007328/AI/NIAID NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Feb 25;463(7284):1042-7. doi: 10.1038/nature08752.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Baxter Laboratory for Stem Cell Biology, Institute for Stem Cell Biology and Regenerative Medicine, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305-5175, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20027182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Fusion ; Cell Line ; Cells, Cultured ; Cellular Reprogramming/genetics/*physiology ; Chromatin Immunoprecipitation ; Cytidine Deaminase/deficiency/genetics/*metabolism ; DNA/chemistry/genetics/metabolism ; *DNA Methylation ; DNA Replication ; Embryonic Stem Cells/cytology/metabolism ; Fibroblasts/cytology/metabolism ; Gene Expression Regulation ; Gene Knockdown Techniques ; Homeodomain Proteins/genetics ; Humans ; Induced Pluripotent Stem Cells/*cytology/enzymology/*metabolism ; Lung/cytology/embryology ; Mice ; Models, Biological ; Octamer Transcription Factor-3/genetics ; Promoter Regions, Genetic/genetics ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Disease-corrected haematopoietic progenitors from Fanconi anaemia induced pluripotent stem cells (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-06-02
    Description: The generation of induced pluripotent stem (iPS) cells has enabled the derivation of patient-specific pluripotent cells and provided valuable experimental platforms to model human disease. Patient-specific iPS cells are also thought to hold great therapeutic potential, although direct evidence for this is still lacking. Here we show that, on correction of the genetic defect, somatic cells from Fanconi anaemia patients can be reprogrammed to pluripotency to generate patient-specific iPS cells. These cell lines appear indistinguishable from human embryonic stem cells and iPS cells from healthy individuals. Most importantly, we show that corrected Fanconi-anaemia-specific iPS cells can give rise to haematopoietic progenitors of the myeloid and erythroid lineages that are phenotypically normal, that is, disease-free. These data offer proof-of-concept that iPS cell technology can be used for the generation of disease-corrected, patient-specific cells with potential value for cell therapy applications.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720823/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720823/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raya, Angel -- Rodriguez-Piza, Ignasi -- Guenechea, Guillermo -- Vassena, Rita -- Navarro, Susana -- Barrero, Maria Jose -- Consiglio, Antonella -- Castella, Maria -- Rio, Paula -- Sleep, Eduard -- Gonzalez, Federico -- Tiscornia, Gustavo -- Garreta, Elena -- Aasen, Trond -- Veiga, Anna -- Verma, Inder M -- Surralles, Jordi -- Bueren, Juan -- Izpisua Belmonte, Juan Carlos -- R01 HL053670/HL/NHLBI NIH HHS/ -- R01 HL053670-14/HL/NHLBI NIH HHS/ -- England -- Nature. 2009 Jul 2;460(7251):53-9. doi: 10.1038/nature08129. Epub 2009 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Regenerative Medicine in Barcelona, Dr. Aiguader 88, 08003 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19483674" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cellular Reprogramming ; Fanconi Anemia/*pathology/*therapy ; Health ; Hematopoietic Stem Cells/*cytology/metabolism ; Humans ; Pluripotent Stem Cells/*cytology/metabolism
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  • 3
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    Frequent inactivation of A20 in B-cell lymphomas (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-05-05
    Description: A20 is a negative regulator of the NF-kappaB pathway and was initially identified as being rapidly induced after tumour-necrosis factor-alpha stimulation. It has a pivotal role in regulation of the immune response and prevents excessive activation of NF-kappaB in response to a variety of external stimuli; recent genetic studies have disclosed putative associations of polymorphic A20 (also called TNFAIP3) alleles with autoimmune disease risk. However, the involvement of A20 in the development of human cancers is unknown. Here we show, using a genome-wide analysis of genetic lesions in 238 B-cell lymphomas, that A20 is a common genetic target in B-lineage lymphomas. A20 is frequently inactivated by somatic mutations and/or deletions in mucosa-associated tissue lymphoma (18 out of 87; 21.8%) and Hodgkin's lymphoma of nodular sclerosis histology (5 out of 15; 33.3%), and, to a lesser extent, in other B-lineage lymphomas. When re-expressed in a lymphoma-derived cell line with no functional A20 alleles, wild-type A20, but not mutant A20, resulted in suppression of cell growth and induction of apoptosis, accompanied by downregulation of NF-kappaB activation. The A20-deficient cells stably generated tumours in immunodeficient mice, whereas the tumorigenicity was effectively suppressed by re-expression of A20. In A20-deficient cells, suppression of both cell growth and NF-kappaB activity due to re-expression of A20 depended, at least partly, on cell-surface-receptor signalling, including the tumour-necrosis factor receptor. Considering the physiological function of A20 in the negative modulation of NF-kappaB activation induced by multiple upstream stimuli, our findings indicate that uncontrolled signalling of NF-kappaB caused by loss of A20 function is involved in the pathogenesis of subsets of B-lineage lymphomas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kato, Motohiro -- Sanada, Masashi -- Kato, Itaru -- Sato, Yasuharu -- Takita, Junko -- Takeuchi, Kengo -- Niwa, Akira -- Chen, Yuyan -- Nakazaki, Kumi -- Nomoto, Junko -- Asakura, Yoshitaka -- Muto, Satsuki -- Tamura, Azusa -- Iio, Mitsuru -- Akatsuka, Yoshiki -- Hayashi, Yasuhide -- Mori, Hiraku -- Igarashi, Takashi -- Kurokawa, Mineo -- Chiba, Shigeru -- Mori, Shigeo -- Ishikawa, Yuichi -- Okamoto, Koji -- Tobinai, Kensei -- Nakagama, Hitoshi -- Nakahata, Tatsutoshi -- Yoshino, Tadashi -- Kobayashi, Yukio -- Ogawa, Seishi -- England -- Nature. 2009 Jun 4;459(7247):712-6. doi: 10.1038/nature07969. Epub 2009 May 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genomics Project, Department of Pediatrics, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19412163" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/physiology ; Cell Line ; Cysteine Endopeptidases/*genetics/*metabolism ; DNA-Binding Proteins ; Gene Expression ; *Gene Silencing ; Genome/genetics ; Humans ; Intracellular Signaling Peptides and Proteins/*genetics/*metabolism ; Lymphoma, B-Cell/*genetics/*physiopathology ; Mice ; NF-kappa B/genetics/metabolism ; Nuclear Proteins/*genetics/*metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Pore architecture and ion sites in acid-sensing ion channels and P2X receptors (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-07-31
    Description: Acid-sensing ion channels are proton-activated, sodium-selective channels composed of three subunits, and are members of the superfamily of epithelial sodium channels, mechanosensitive and FMRF-amide peptide-gated ion channels. These ubiquitous eukaryotic ion channels have essential roles in biological activities as diverse as sodium homeostasis, taste and pain. Despite their crucial roles in biology and their unusual trimeric subunit stoichiometry, there is little knowledge of the structural and chemical principles underlying their ion channel architecture and ion-binding sites. Here we present the structure of a functional acid-sensing ion channel in a desensitized state at 3 A resolution, the location and composition of the approximately 8 A 'thick' desensitization gate, and the trigonal antiprism coordination of caesium ions bound in the extracellular vestibule. Comparison of the acid-sensing ion channel structure with the ATP-gated P2X(4) receptor reveals similarity in pore architecture and aqueous vestibules, suggesting that there are unanticipated yet common structural and mechanistic principles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845979/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845979/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gonzales, Eric B -- Kawate, Toshimitsu -- Gouaux, Eric -- F32 GM083615/GM/NIGMS NIH HHS/ -- F32 GM083615-01/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jul 30;460(7255):599-604. doi: 10.1038/nature08218.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97239, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19641589" target="_blank"〉PubMed〈/a〉
    Keywords: Acid Sensing Ion Channels ; Animals ; Binding Sites ; CHO Cells ; Cell Line ; Cesium/metabolism ; Chickens/*physiology ; Cricetinae ; Cricetulus ; Crystallization ; Humans ; Ions/metabolism ; *Models, Molecular ; Nerve Tissue Proteins/*chemistry ; Protein Structure, Tertiary ; Receptors, Purinergic P2/*chemistry ; Receptors, Purinergic P2X ; Sodium Channels/*chemistry ; Zebrafish/*physiology
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  • 5
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    Zc3h12a is an RNase essential for controlling immune responses by regulating mRNA decay (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-03-27
    Description: Toll-like receptors (TLRs) recognize microbial components, and evoke inflammation and immune responses. TLR stimulation activates complex gene expression networks that regulate the magnitude and duration of the immune reaction. Here we identify the TLR-inducible gene Zc3h12a as an immune response modifier that has an essential role in preventing immune disorders. Zc3h12a-deficient mice suffered from severe anaemia, and most died within 12 weeks. Zc3h12a(-/-) mice also showed augmented serum immunoglobulin levels and autoantibody production, together with a greatly increased number of plasma cells, as well as infiltration of plasma cells to the lung. Most Zc3h12a(-/-) splenic T cells showed effector/memory characteristics and produced interferon-gamma in response to T-cell receptor stimulation. Macrophages from Zc3h12a(-/-) mice showed highly increased production of interleukin (IL)-6 and IL-12p40 (also known as IL12b), but not TNF, in response to TLR ligands. Although the activation of TLR signalling pathways was normal, Il6 messenger RNA decay was severely impaired in Zc3h12a(-/-) macrophages. Overexpression of Zc3h12a accelerated Il6 mRNA degradation via its 3'-untranslated region (UTR), and destabilized RNAs with 3'-UTRs for genes including Il6, Il12p40 and the calcitonin receptor gene Calcr. Zc3h12a contains a putative amino-terminal nuclease domain, and the expressed protein had RNase activity, consistent with a role in the decay of Il6 mRNA. Together, these results indicate that Zc3h12a is an essential RNase that prevents immune disorders by directly controlling the stability of a set of inflammatory genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsushita, Kazufumi -- Takeuchi, Osamu -- Standley, Daron M -- Kumagai, Yutaro -- Kawagoe, Tatsukata -- Miyake, Tohru -- Satoh, Takashi -- Kato, Hiroki -- Tsujimura, Tohru -- Nakamura, Haruki -- Akira, Shizuo -- P01 AI070167/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Apr 30;458(7242):1185-90. doi: 10.1038/nature07924. Epub 2009 Mar 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19322177" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics/metabolism ; Anemia/complications/genetics ; Animals ; Autoantibodies/blood/immunology ; Autoimmune Diseases/complications/immunology ; Cell Line ; Cytokines/biosynthesis/genetics ; Fetal Diseases/immunology ; Humans ; Immunity/*genetics/*immunology ; Inflammation Mediators/metabolism ; Interleukin-6/genetics ; Macrophages, Peritoneal/immunology/metabolism ; Mice ; Plasma Cells/cytology ; *RNA Stability ; Ribonucleases/deficiency/genetics/*metabolism ; T-Lymphocytes/immunology
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  • 6
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    HMGB proteins function as universal sentinels for nucleic-acid-mediated innate immune responses (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-11-06
    Description: The activation of innate immune responses by nucleic acids is crucial to protective and pathological immunities and is mediated by the transmembrane Toll-like receptors (TLRs) and cytosolic receptors. However, it remains unknown whether a mechanism exists that integrates these nucleic-acid-sensing systems. Here we show that high-mobility group box (HMGB) proteins 1, 2 and 3 function as universal sentinels for nucleic acids. HMGBs bind to all immunogenic nucleic acids examined with a correlation between affinity and immunogenic potential. Hmgb1(-/-) and Hmgb2(-/-) mouse cells are defective in type-I interferon and inflammatory cytokine induction by DNA or RNA targeted to activate the cytosolic nucleic-acid-sensing receptors; cells in which the expression of all three HMGBs is suppressed show a more profound defect, accompanied by impaired activation of the transcription factors interferon regulatory factor 3 (IRF3) and nuclear factor (NF)-kappaB. The absence of HMGBs also severely impairs the activation of TLR3, TLR7 and TLR9 by their cognate nucleic acids. Our results therefore indicate a hierarchy in the nucleic-acid-mediated activation of immune responses, wherein the selective activation of nucleic-acid-sensing receptors is contingent on the more promiscuous sensing of nucleic acids by HMGBs. These findings may have implications for understanding the evolution of the innate immune system and for the treatment of immunological disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yanai, Hideyuki -- Ban, Tatsuma -- Wang, ZhiChao -- Choi, Myoung Kwon -- Kawamura, Takeshi -- Negishi, Hideo -- Nakasato, Makoto -- Lu, Yan -- Hangai, Sho -- Koshiba, Ryuji -- Savitsky, David -- Ronfani, Lorenza -- Akira, Shizuo -- Bianchi, Marco E -- Honda, Kenya -- Tamura, Tomohiko -- Kodama, Tatsuhiko -- Taniguchi, Tadatsugu -- England -- Nature. 2009 Nov 5;462(7269):99-103. doi: 10.1038/nature08512.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19890330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cytosol/immunology ; DNA/immunology ; HMGB Proteins/deficiency/genetics/*immunology/*metabolism ; HMGB1 Protein/deficiency/genetics/immunology/metabolism ; HMGB2 Protein/deficiency/genetics/immunology/metabolism ; Immunity, Innate/*immunology ; Interferon Regulatory Factor-3/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Immunological ; NF-kappa B/metabolism ; Nucleic Acids/*immunology ; Nucleotides/chemistry/immunology/metabolism ; RNA/immunology ; Signal Transduction ; Toll-Like Receptors/immunology ; Virus Diseases/immunology/virology
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  • 7
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    Cancer-associated IDH1 mutations produce 2-hydroxyglutarate (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-11-26
    Description: Mutations in the enzyme cytosolic isocitrate dehydrogenase 1 (IDH1) are a common feature of a major subset of primary human brain cancers. These mutations occur at a single amino acid residue of the IDH1 active site, resulting in loss of the enzyme's ability to catalyse conversion of isocitrate to alpha-ketoglutarate. However, only a single copy of the gene is mutated in tumours, raising the possibility that the mutations do not result in a simple loss of function. Here we show that cancer-associated IDH1 mutations result in a new ability of the enzyme to catalyse the NADPH-dependent reduction of alpha-ketoglutarate to R(-)-2-hydroxyglutarate (2HG). Structural studies demonstrate that when arginine 132 is mutated to histidine, residues in the active site are shifted to produce structural changes consistent with reduced oxidative decarboxylation of isocitrate and acquisition of the ability to convert alpha-ketoglutarate to 2HG. Excess accumulation of 2HG has been shown to lead to an elevated risk of malignant brain tumours in patients with inborn errors of 2HG metabolism. Similarly, in human malignant gliomas harbouring IDH1 mutations, we find markedly elevated levels of 2HG. These data demonstrate that the IDH1 mutations result in production of the onco-metabolite 2HG, and indicate that the excess 2HG which accumulates in vivo contributes to the formation and malignant progression of gliomas.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2818760/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2818760/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dang, Lenny -- White, David W -- Gross, Stefan -- Bennett, Bryson D -- Bittinger, Mark A -- Driggers, Edward M -- Fantin, Valeria R -- Jang, Hyun Gyung -- Jin, Shengfang -- Keenan, Marie C -- Marks, Kevin M -- Prins, Robert M -- Ward, Patrick S -- Yen, Katharine E -- Liau, Linda M -- Rabinowitz, Joshua D -- Cantley, Lewis C -- Thompson, Craig B -- Vander Heiden, Matthew G -- Su, Shinsan M -- P01 CA104838/CA/NCI NIH HHS/ -- P01 CA104838-05/CA/NCI NIH HHS/ -- P30 EB009998/EB/NIBIB NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- R01 CA105463-06/CA/NCI NIH HHS/ -- R21 CA128620/CA/NCI NIH HHS/ -- England -- Nature. 2009 Dec 10;462(7274):739-44. doi: 10.1038/nature08617. Epub .〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Agios Pharmaceuticals, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19935646" target="_blank"〉PubMed〈/a〉
    Keywords: Arginine/genetics ; Brain Neoplasms/*genetics/*metabolism/pathology ; Catalytic Domain ; Cell Line ; Crystallography, X-Ray ; Disease Progression ; Enzyme Assays ; Glioma/genetics/metabolism/pathology ; Glutarates/*metabolism ; Histidine/genetics/metabolism ; Humans ; Isocitrate Dehydrogenase/*genetics/*metabolism ; Ketoglutaric Acids/metabolism ; Models, Molecular ; Mutant Proteins/*genetics/*metabolism ; Mutation/genetics ; Protein Conformation
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  • 8
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    Malaria: The gatekeeper revealed (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-06-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reiff, Sarah B -- Striepen, Boris -- England -- Nature. 2009 Jun 18;459(7249):918-9. doi: 10.1038/459918a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19536248" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Malaria, Falciparum/drug therapy/*parasitology ; Models, Biological ; Plasmodium falciparum/*metabolism ; Protein Binding ; Protein Transport ; Protozoan Proteins/antagonists & inhibitors/*metabolism ; Vacuoles/metabolism/parasitology
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    Modulation of microRNA processing by p53 (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-07-25
    Description: MicroRNAs (miRNAs) have emerged as key post-transcriptional regulators of gene expression, involved in diverse physiological and pathological processes. Although miRNAs can function as both tumour suppressors and oncogenes in tumour development, a widespread downregulation of miRNAs is commonly observed in human cancers and promotes cellular transformation and tumorigenesis. This indicates an inherent significance of small RNAs in tumour suppression. However, the connection between tumour suppressor networks and miRNA biogenesis machineries has not been investigated in depth. Here we show that a central tumour suppressor, p53, enhances the post-transcriptional maturation of several miRNAs with growth-suppressive function, including miR-16-1, miR-143 and miR-145, in response to DNA damage. In HCT116 cells and human diploid fibroblasts, p53 interacts with the Drosha processing complex through the association with DEAD-box RNA helicase p68 (also known as DDX5) and facilitates the processing of primary miRNAs to precursor miRNAs. We also found that transcriptionally inactive p53 mutants interfere with a functional assembly between Drosha complex and p68, leading to attenuation of miRNA processing activity. These findings suggest that transcription-independent modulation of miRNA biogenesis is intrinsically embedded in a tumour suppressive program governed by p53. Our study reveals a previously unrecognized function of p53 in miRNA processing, which may underlie key aspects of cancer biology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, Hiroshi I -- Yamagata, Kaoru -- Sugimoto, Koichi -- Iwamoto, Takashi -- Kato, Shigeaki -- Miyazono, Kohei -- England -- Nature. 2009 Jul 23;460(7254):529-33. doi: 10.1038/nature08199.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19626115" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; DNA Damage/physiology ; Gene Expression Regulation ; HCT116 Cells ; Humans ; MicroRNAs/*metabolism ; Mutation ; *RNA Processing, Post-Transcriptional ; Ribonuclease III/metabolism ; Tumor Suppressor Protein p53/genetics/*metabolism
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    Human DAZL, DAZ and BOULE genes modulate primordial germ-cell and haploid gamete formation (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-10-30
    Description: The leading cause of infertility in men and women is quantitative and qualitative defects in human germ-cell (oocyte and sperm) development. Yet, it has not been possible to examine the unique developmental genetics of human germ-cell formation and differentiation owing to inaccessibility of germ cells during fetal development. Although several studies have shown that germ cells can be differentiated from mouse and human embryonic stem cells, human germ cells differentiated in these studies generally did not develop beyond the earliest stages. Here we used a germ-cell reporter to quantify and isolate primordial germ cells derived from both male and female human embryonic stem cells. By silencing and overexpressing genes that encode germ-cell-specific cytoplasmic RNA-binding proteins (not transcription factors), we modulated human germ-cell formation and developmental progression. We observed that human DAZL (deleted in azoospermia-like) functions in primordial germ-cell formation, whereas closely related genes DAZ and BOULE (also called BOLL) promote later stages of meiosis and development of haploid gametes. These results are significant to the generation of gametes for future basic science and potential clinical applications.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3133736/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3133736/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kee, Kehkooi -- Angeles, Vanessa T -- Flores, Martha -- Nguyen, Ha Nam -- Reijo Pera, Renee A -- R01 HD047721/HD/NICHD NIH HHS/ -- R01 HD047721-06/HD/NICHD NIH HHS/ -- R01HD047721/HD/NICHD NIH HHS/ -- U54 HD055764/HD/NICHD NIH HHS/ -- U54 HD055764-015755/HD/NICHD NIH HHS/ -- U54HD055764/HD/NICHD NIH HHS/ -- England -- Nature. 2009 Nov 12;462(7270):222-5. doi: 10.1038/nature08562. Epub 2009 Oct 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Human Embryonic Stem Cell Research and Education, Institute for Stem Cell Biology & Regenerative Medicine, Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford University, Palo Alto, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19865085" target="_blank"〉PubMed〈/a〉
    Keywords: Bone Morphogenetic Proteins/metabolism ; Cell Count ; *Cell Differentiation ; Cell Line ; Cellular Reprogramming ; Embryonic Stem Cells/cytology/metabolism ; Female ; Gene Expression ; Gene Silencing ; Genes, Reporter ; Germ Cells/*cytology/*metabolism ; *Haploidy ; Humans ; Male ; Meiosis ; Organ Specificity ; RNA-Binding Proteins/genetics/*metabolism
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    Crystal structure of the ATP-gated P2X(4) ion channel in the closed state (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-07-31
    Description: P2X receptors are cation-selective ion channels gated by extracellular ATP, and are implicated in diverse physiological processes, from synaptic transmission to inflammation to the sensing of taste and pain. Because P2X receptors are not related to other ion channel proteins of known structure, there is at present no molecular foundation for mechanisms of ligand-gating, allosteric modulation and ion permeation. Here we present crystal structures of the zebrafish P2X(4) receptor in its closed, resting state. The chalice-shaped, trimeric receptor is knit together by subunit-subunit contacts implicated in ion channel gating and receptor assembly. Extracellular domains, rich in beta-strands, have large acidic patches that may attract cations, through fenestrations, to vestibules near the ion channel. In the transmembrane pore, the 'gate' is defined by an approximately 8 A slab of protein. We define the location of three non-canonical, intersubunit ATP-binding sites, and suggest that ATP binding promotes subunit rearrangement and ion channel opening.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720809/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720809/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawate, Toshimitsu -- Michel, Jennifer Carlisle -- Birdsong, William T -- Gouaux, Eric -- U54 GM075026/GM/NIGMS NIH HHS/ -- U54 GM075026-04/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jul 30;460(7255):592-8. doi: 10.1038/nature08198.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, Oregon 97239, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19641588" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; Cell Line ; Crystallography, X-Ray ; Gadolinium/metabolism ; Humans ; Ion Channels/antagonists & inhibitors/*chemistry ; Membrane Proteins/chemistry ; *Models, Molecular ; Protein Binding ; Protein Folding ; Protein Structure, Tertiary ; Purinergic P2 Receptor Antagonists ; Receptors, Purinergic P2/*chemistry ; Receptors, Purinergic P2X4 ; Zebrafish/*physiology ; Zebrafish Proteins/antagonists & inhibitors/*chemistry
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    CBP/p300-mediated acetylation of histone H3 on lysine 56 (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-03-10
    Description: Acetylation within the globular core domain of histone H3 on lysine 56 (H3K56) has recently been shown to have a critical role in packaging DNA into chromatin following DNA replication and repair in budding yeast. However, the function or occurrence of this specific histone mark has not been studied in multicellular eukaryotes, mainly because the Rtt109 enzyme that is known to mediate acetylation of H3K56 (H3K56ac) is fungal-specific. Here we demonstrate that the histone acetyl transferase CBP (also known as Nejire) in flies and CBP and p300 (Ep300) in humans acetylate H3K56, whereas Drosophila Sir2 and human SIRT1 and SIRT2 deacetylate H3K56ac. The histone chaperones ASF1A in humans and Asf1 in Drosophila are required for acetylation of H3K56 in vivo, whereas the histone chaperone CAF-1 (chromatin assembly factor 1) in humans and Caf1 in Drosophila are required for the incorporation of histones bearing this mark into chromatin. We show that, in response to DNA damage, histones bearing acetylated K56 are assembled into chromatin in Drosophila and human cells, forming foci that colocalize with sites of DNA repair. Furthermore, acetylation of H3K56 is increased in multiple types of cancer, correlating with increased levels of ASF1A in these tumours. Our identification of multiple proteins regulating the levels of H3K56 acetylation in metazoans will allow future studies of this critical and unique histone modification that couples chromatin assembly to DNA synthesis, cell proliferation and cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756583/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756583/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Das, Chandrima -- Lucia, M Scott -- Hansen, Kirk C -- Tyler, Jessica K -- CA95641/CA/NCI NIH HHS/ -- GM64475/GM/NIGMS NIH HHS/ -- R01 CA095641/CA/NCI NIH HHS/ -- R01 CA095641-07/CA/NCI NIH HHS/ -- R01 GM064475/GM/NIGMS NIH HHS/ -- R01 GM064475-07/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 May 7;459(7243):113-7. doi: 10.1038/nature07861. Epub 2009 Mar 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, PO Box 6511, Aurora Colorado 80045, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19270680" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Cell Cycle Proteins/metabolism ; Cell Line ; Chromosomal Proteins, Non-Histone/metabolism ; DNA Damage/physiology ; Drosophila Proteins/metabolism ; Drosophila melanogaster/*enzymology ; HeLa Cells ; Histone Deacetylases/metabolism ; Histones/*metabolism ; Humans ; Lysine/*metabolism ; Molecular Chaperones/metabolism ; Retinoblastoma-Binding Protein 4 ; Sirtuin 1 ; Sirtuin 2 ; Sirtuins/metabolism ; p300-CBP Transcription Factors/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Riboflavin kinase couples TNF receptor 1 to NADPH oxidase (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-07-31
    Description: Reactive oxygen species (ROS) produced by NADPH oxidase function as defence and signalling molecules related to innate immunity and various cellular responses. The activation of NADPH oxidase in response to plasma membrane receptor activation depends on the phosphorylation of cytoplasmic oxidase subunits, their translocation to membranes and the assembly of all NADPH oxidase components. Tumour necrosis factor (TNF) is a prominent stimulus of ROS production, but the molecular mechanisms by which TNF activates NADPH oxidase are poorly understood. Here we identify riboflavin kinase (RFK, formerly known as flavokinase) as a previously unrecognized TNF-receptor-1 (TNFR1)-binding protein that physically and functionally couples TNFR1 to NADPH oxidase. In mouse and human cells, RFK binds to both the TNFR1-death domain and to p22(phox), the common subunit of NADPH oxidase isoforms. RFK-mediated bridging of TNFR1 and p22(phox) is a prerequisite for TNF-induced but not for Toll-like-receptor-induced ROS production. Exogenous flavin mononucleotide or FAD was able to substitute fully for TNF stimulation of NADPH oxidase in RFK-deficient cells. RFK is rate-limiting in the synthesis of FAD, an essential prosthetic group of NADPH oxidase. The results suggest that TNF, through the activation of RFK, enhances the incorporation of FAD in NADPH oxidase enzymes, a critical step for the assembly and activation of NADPH oxidase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yazdanpanah, Benjamin -- Wiegmann, Katja -- Tchikov, Vladimir -- Krut, Oleg -- Pongratz, Carola -- Schramm, Michael -- Kleinridders, Andre -- Wunderlich, Thomas -- Kashkar, Hamid -- Utermohlen, Olaf -- Bruning, Jens C -- Schutze, Stefan -- Kronke, Martin -- England -- Nature. 2009 Aug 27;460(7259):1159-63. doi: 10.1038/nature08206. Epub 2009 Jul 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19641494" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cytochrome b Group/metabolism ; Enzyme Activation ; Fibroblasts ; Flavin Mononucleotide/metabolism ; Flavin-Adenine Dinucleotide/biosynthesis/metabolism ; HeLa Cells ; Humans ; Isoenzymes/chemistry/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; NADH, NADPH Oxidoreductases/metabolism ; NADPH Oxidase/chemistry/*metabolism ; Phosphotransferases (Alcohol Group Acceptor)/deficiency/genetics/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; Reactive Oxygen Species/metabolism ; Receptors, Tumor Necrosis Factor, Type I/chemistry/*metabolism
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    MicroRNA-mediated switching of chromatin-remodelling complexes in neural development (2009)
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    Publication Date: 2009-06-30
    Description: One of the most distinctive steps in the development of the vertebrate nervous system occurs at mitotic exit when cells lose multipotency and begin to develop stable connections that will persist for a lifetime. This transition is accompanied by a switch in ATP-dependent chromatin-remodelling mechanisms that appears to coincide with the final mitotic division of neurons. This switch involves the exchange of the BAF53a (also known as ACTL6a) and BAF45a (PHF10) subunits within Swi/Snf-like neural-progenitor-specific BAF (npBAF) complexes for the homologous BAF53b (ACTL6b) and BAF45b (DPF1) subunits within neuron-specific BAF (nBAF) complexes in post-mitotic neurons. The subunits of the npBAF complex are essential for neural-progenitor proliferation, and mice with reduced dosage for the genes encoding its subunits have defects in neural-tube closure similar to those in human spina bifida, one of the most serious congenital birth defects. In contrast, BAF53b and the nBAF complex are essential for an evolutionarily conserved program of post-mitotic neural development and dendritic morphogenesis. Here we show that this essential transition is mediated by repression of BAF53a by miR-9* and miR-124. We find that BAF53a repression is mediated by sequences in the 3' untranslated region corresponding to the recognition sites for miR-9* and miR-124, which are selectively expressed in post-mitotic neurons. Mutation of these sites led to persistent expression of BAF53a and defective activity-dependent dendritic outgrowth in neurons. In addition, overexpression of miR-9* and miR-124 in neural progenitors caused reduced proliferation. Previous studies have indicated that miR-9* and miR-124 are repressed by the repressor-element-1-silencing transcription factor (REST, also known as NRSF). Indeed, expression of REST in post-mitotic neurons led to derepression of BAF53a, indicating that REST-mediated repression of microRNAs directs the essential switch of chromatin regulatory complexes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2921580/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2921580/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoo, Andrew S -- Staahl, Brett T -- Chen, Lei -- Crabtree, Gerald R -- 2 T32 HD007249/HD/NICHD NIH HHS/ -- AI060037/AI/NIAID NIH HHS/ -- HD55391/HD/NICHD NIH HHS/ -- NS046789/NS/NINDS NIH HHS/ -- R01 HD055391/HD/NICHD NIH HHS/ -- R01 NS046789/NS/NINDS NIH HHS/ -- R01 NS046789-08/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jul 30;460(7255):642-6. doi: 10.1038/nature08139. Epub 2009 Jun 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, and Department of Developmental Biology, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19561591" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/metabolism ; Actins/genetics/metabolism ; Animals ; CHO Cells ; Cell Line ; Chromatin Assembly and Disassembly/genetics/*physiology ; Chromosomal Proteins, Non-Histone/genetics/metabolism ; Cricetinae ; Cricetulus ; DNA-Binding Proteins/genetics/metabolism ; Dendrites/physiology ; *Gene Expression Regulation, Developmental ; Mice ; Mice, Transgenic ; MicroRNAs/*metabolism ; Mitosis ; Nervous System/cytology/*embryology ; Neurons/cytology ; Repressor Proteins/metabolism ; Stem Cells/metabolism
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    Human ISL1 heart progenitors generate diverse multipotent cardiovascular cell lineages (2009)
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    Publication Date: 2009-07-03
    Description: The generation and expansion of diverse cardiovascular cell lineages is a critical step during human cardiogenesis, with major implications for congenital heart disease. Unravelling the mechanisms for the diversification of human heart cell lineages has been hampered by the lack of genetic tools to purify early cardiac progenitors and define their developmental potential. Recent studies in the mouse embryo have identified a multipotent cardiac progenitor that contributes to all of the major cell types in the murine heart. In contrast to murine development, human cardiogenesis has a much longer onset of heart cell lineage diversification and expansion, suggesting divergent pathways. Here we identify a diverse set of human fetal ISL1(+) cardiovascular progenitors that give rise to the cardiomyocyte, smooth muscle and endothelial cell lineages. Using two independent transgenic and gene-targeting approaches in human embryonic stem cell lines, we show that purified ISL1(+) primordial progenitors are capable of self-renewal and expansion before differentiation into the three major cell types in the heart. These results lay the foundation for the generation of human model systems for cardiovascular disease and novel approaches for human regenerative cardiovascular medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bu, Lei -- Jiang, Xin -- Martin-Puig, Silvia -- Caron, Leslie -- Zhu, Shenjun -- Shao, Ying -- Roberts, Drucilla J -- Huang, Paul L -- Domian, Ibrahim J -- Chien, Kenneth R -- England -- Nature. 2009 Jul 2;460(7251):113-7. doi: 10.1038/nature08191.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Center, Massachusetts General Hospital, Charles River Plaza/CPZN 3208, 185 Cambridge Street, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19571884" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation ; Cell Division ; Cell Line ; *Cell Lineage ; Coculture Techniques ; Embryonic Stem Cells/cytology/metabolism ; Endothelial Cells/cytology ; Fetus/cytology/embryology ; Heart/embryology ; Homeodomain Proteins/*metabolism ; Humans ; LIM-Homeodomain Proteins ; Multipotent Stem Cells/*cytology/*metabolism ; Muscle, Smooth/cytology ; Myocardium/*cytology ; Myocytes, Cardiac/cytology ; Transcription Factors ; Wnt Proteins/metabolism ; Wnt3 Protein
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    Growth landscape formed by perception and import of glucose in yeast (2009)
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    Publication Date: 2009-12-18
    Description: An important challenge in systems biology is to quantitatively describe microbial growth using a few measurable parameters that capture the essence of this complex phenomenon. Two key events at the cell membrane-extracellular glucose sensing and uptake-initiate the budding yeast's growth on glucose. However, conventional growth models focus almost exclusively on glucose uptake. Here we present results from growth-rate experiments that cannot be explained by focusing on glucose uptake alone. By imposing a glucose uptake rate independent of the sensed extracellular glucose level, we show that despite increasing both the sensed glucose concentration and uptake rate, the cell's growth rate can decrease or even approach zero. We resolve this puzzle by showing that the interaction between glucose perception and import, not their individual actions, determines the central features of growth, and characterize this interaction using a quantitative model. Disrupting this interaction by knocking out two key glucose sensors significantly changes the cell's growth rate, yet uptake rates are unchanged. This is due to a decrease in burden that glucose perception places on the cells. Our work shows that glucose perception and import are separate and pivotal modules of yeast growth, the interaction of which can be precisely tuned and measured.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796206/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796206/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Youk, Hyun -- van Oudenaarden, Alexander -- DP1 OD003936/OD/NIH HHS/ -- DP1 OD003936-01/OD/NIH HHS/ -- DP1 OD003936-02/OD/NIH HHS/ -- R01 GM068957/GM/NIGMS NIH HHS/ -- R01 GM068957-06/GM/NIGMS NIH HHS/ -- R01 GM068957-07/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Dec 17;462(7275):875-9. doi: 10.1038/nature08653.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016593" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Transport/drug effects ; Cell Growth Processes/drug effects ; Cell Membrane/drug effects/metabolism ; Doxycycline/pharmacology ; Glucose/*metabolism/pharmacology ; Kinetics ; Models, Biological ; Saccharomyces cerevisiae/cytology/drug effects/*growth & development/*metabolism
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    JAK2 phosphorylates histone H3Y41 and excludes HP1alpha from chromatin (2009)
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    Publication Date: 2009-09-29
    Description: Activation of Janus kinase 2 (JAK2) by chromosomal translocations or point mutations is a frequent event in haematological malignancies. JAK2 is a non-receptor tyrosine kinase that regulates several cellular processes by inducing cytoplasmic signalling cascades. Here we show that human JAK2 is present in the nucleus of haematopoietic cells and directly phosphorylates Tyr 41 (Y41) on histone H3. Heterochromatin protein 1alpha (HP1alpha), but not HP1beta, specifically binds to this region of H3 through its chromo-shadow domain. Phosphorylation of H3Y41 by JAK2 prevents this binding. Inhibition of JAK2 activity in human leukaemic cells decreases both the expression of the haematopoietic oncogene lmo2 and the phosphorylation of H3Y41 at its promoter, while simultaneously increasing the binding of HP1alpha at the same site. Tauhese results identify a previously unrecognized nuclear role for JAK2 in the phosphorylation of H3Y41 and reveal a direct mechanistic link between two genes, jak2 and lmo2, involved in normal haematopoiesis and leukaemia.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3785147/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3785147/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, Mark A -- Bannister, Andrew J -- Gottgens, Berthold -- Foster, Samuel D -- Bartke, Till -- Green, Anthony R -- Kouzarides, Tony -- 089957/Wellcome Trust/United Kingdom -- 12765/Cancer Research UK/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- MC_UP_1102/2/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2009 Oct 8;461(7265):819-22. doi: 10.1038/nature08448. Epub 2009 Sep 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cambridge Institute for Medical Research and Department of Haematology, University of Cambridge, Hills Road, Cambridge CB2 0XY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19783980" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Binding Sites ; Cell Line ; Cell Nucleus/enzymology ; Chromatin/chemistry/*metabolism ; Chromosomal Proteins, Non-Histone/*metabolism ; DNA-Binding Proteins/genetics ; Gene Expression Regulation, Neoplastic ; Hematopoiesis/genetics ; Hematopoietic Stem Cells/cytology/enzymology ; Histones/chemistry/genetics/*metabolism ; Humans ; Janus Kinase 2/antagonists & inhibitors/*metabolism ; LIM Domain Proteins ; Leukemia/enzymology/genetics/metabolism/pathology ; Metalloproteins/genetics ; Mice ; Oncogenes/genetics ; Phosphorylation ; Promoter Regions, Genetic/genetics ; Protein Binding ; Proto-Oncogene Proteins ; Signal Transduction ; Tyrosine/metabolism
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    Fgf8 morphogen gradient forms by a source-sink mechanism with freely diffusing molecules (2009)
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    Details
    Publication Date: 2009-09-11
    Description: It is widely accepted that tissue differentiation and morphogenesis in multicellular organisms are regulated by tightly controlled concentration gradients of morphogens. How exactly these gradients are formed, however, remains unclear. Here we show that Fgf8 morphogen gradients in living zebrafish embryos are established and maintained by two essential factors: fast, free diffusion of single molecules away from the source through extracellular space, and a sink function of the receiving cells, regulated by receptor-mediated endocytosis. Evidence is provided by directly examining single molecules of Fgf8 in living tissue by fluorescence correlation spectroscopy, quantifying their local mobility and concentration with high precision. By changing the degree of uptake of Fgf8 into its target cells, we are able to alter the shape of the Fgf8 gradient. Our results demonstrate that a freely diffusing morphogen can set up concentration gradients in a complex multicellular tissue by a simple source-sink mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Shuizi Rachel -- Burkhardt, Markus -- Nowak, Matthias -- Ries, Jonas -- Petrasek, Zdenek -- Scholpp, Steffen -- Schwille, Petra -- Brand, Michael -- England -- Nature. 2009 Sep 24;461(7263):533-6. doi: 10.1038/nature08391. Epub 2009 Sep 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Genetics, Biotechnology Center, TUD, Tatzberg 47-49, 01307 Dresden, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19741606" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diffusion ; Embryo, Nonmammalian/*cytology/embryology/*metabolism ; *Endocytosis ; Extracellular Space/metabolism ; Fibroblast Growth Factors/genetics/*metabolism ; Gastrulation ; Green Fluorescent Proteins/genetics/metabolism ; Models, Biological ; Morphogenesis/*physiology ; Receptors, Fibroblast Growth Factor/metabolism ; Zebrafish/*embryology/*metabolism ; Zebrafish Proteins/genetics/*metabolism
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    Formyl peptide receptor-like proteins are a novel family of vomeronasal chemosensors (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-04-24
    Description: Mammals rely heavily on olfaction to interact adequately with each other and with their environment. They make use of seven-transmembrane G-protein-coupled receptors to identify odorants and pheromones. These receptors are present on dendrites of olfactory sensory neurons located in the main olfactory or vomeronasal sensory epithelia, and pertain to the odorant, trace amine-associated receptor and vomeronasal type 1 (ref. 4) or 2 (refs 5-7) receptor superfamilies. Whether these four sensor classes represent the complete olfactory molecular repertoire used by mammals to make sense of the outside world is unknown. Here we report the expression of formyl peptide receptor-related genes by vomeronasal sensory neurons, in multiple mammalian species. Similar to the four known olfactory receptor gene classes, these genes encode seven-transmembrane proteins, and are characterized by monogenic transcription and a punctate expression pattern in the sensory neuroepithelium. In vitro expression of mouse formyl peptide receptor-like 1, 3, 4, 6 and 7 provides sensitivity to disease/inflammation-related ligands. Establishing an in situ approach that combines whole-mount vomeronasal preparations with dendritic calcium imaging in the intact neuroepithelium, we show neuronal responses to the same molecules, which therefore represent a new class of vomeronasal agonists. Taken together, these results suggest that formyl peptide receptor-like proteins have an olfactory function associated with the identification of pathogens, or of pathogenic states.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riviere, Stephane -- Challet, Ludivine -- Fluegge, Daniela -- Spehr, Marc -- Rodriguez, Ivan -- England -- Nature. 2009 May 28;459(7246):574-7. doi: 10.1038/nature08029.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology and Animal Biology, and National Center of Competence Frontiers in Genetics, University of Geneva, 1205 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19387439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium Signaling ; Cell Line ; Dendrites/drug effects/metabolism ; *Disease ; Gene Expression Profiling ; Humans ; Inflammation/pathology ; Ligands ; Mice ; Olfactory Perception/drug effects/*physiology ; Olfactory Receptor Neurons/cytology/drug effects/*metabolism ; Organ Specificity ; Receptors, Formyl Peptide/genetics/*metabolism ; Smell/drug effects/*physiology ; Vomeronasal Organ/*cytology/drug effects/physiology
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    Direct reprogramming of human neural stem cells by OCT4 (2009)
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    Publication Date: 2009-09-01
    Description: Induced pluripotent stem (iPS) cells have been generated from mouse and human somatic cells by ectopic expression of four transcription factors (OCT4 (also called POU5F1), SOX2, c-Myc and KLF4). We previously reported that Oct4 alone is sufficient to reprogram directly adult mouse neural stem cells to iPS cells. Here we report the generation of one-factor human iPS cells from human fetal neural stem cells (one-factor (1F) human NiPS cells) by ectopic expression of OCT4 alone. One-factor human NiPS cells resemble human embryonic stem cells in global gene expression profiles, epigenetic status, as well as pluripotency in vitro and in vivo. These findings demonstrate that the transcription factor OCT4 is sufficient to reprogram human neural stem cells to pluripotency. One-factor iPS cell generation will advance the field further towards understanding reprogramming and generating patient-specific pluripotent stem cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jeong Beom -- Greber, Boris -- Arauzo-Bravo, Marcos J -- Meyer, Johann -- Park, Kook In -- Zaehres, Holm -- Scholer, Hans R -- England -- Nature. 2009 Oct 1;461(7264):649-3. doi: 10.1038/nature08436.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Molecular Biomedicine, Department of Cell and Developmental Biology, Rontgenstrasse 20, 48149 Munster, NRW, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19718018" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; *Cell Dedifferentiation ; Cell Differentiation ; Cell Line ; *Cellular Reprogramming ; DNA Methylation ; Embryonic Stem Cells/cytology/metabolism ; Epigenesis, Genetic ; Fetus/*cytology ; Gene Expression Profiling ; Germ Layers/cytology/metabolism ; Humans ; Mice ; Neurons/*cytology/metabolism ; Octamer Transcription Factor-3/genetics/*metabolism ; Pluripotent Stem Cells/*cytology/*metabolism
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    Requirement for NF-kappaB signalling in a mouse model of lung adenocarcinoma (2009)
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    Publication Date: 2009-10-23
    Description: NF-kappaB transcription factors function as crucial regulators of inflammatory and immune responses as well as of cell survival. They have also been implicated in cellular transformation and tumorigenesis. However, despite extensive biochemical characterization of NF-kappaB signalling during the past twenty years, the requirement for NF-kappaB in tumour development in vivo, particularly in solid tumours, is not completely understood. Here we show that the NF-kappaB pathway is required for the development of tumours in a mouse model of lung adenocarcinoma. Concomitant loss of p53 (also known as Trp53) and expression of oncogenic Kras(G12D) resulted in NF-kappaB activation in primary mouse embryonic fibroblasts. Conversely, in lung tumour cell lines expressing Kras(G12D) and lacking p53, p53 restoration led to NF-kappaB inhibition. Furthermore, the inhibition of NF-kappaB signalling induced apoptosis in p53-null lung cancer cell lines. Inhibition of the pathway in lung tumours in vivo, from the time of tumour initiation or after tumour progression, resulted in significantly reduced tumour development. Together, these results indicate a critical function for NF-kappaB signalling in lung tumour development and, further, that this requirement depends on p53 status. These findings also provide support for the development of NF-kappaB inhibitory drugs as targeted therapies for the treatment of patients with defined mutations in Kras and p53.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780341/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780341/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meylan, Etienne -- Dooley, Alison L -- Feldser, David M -- Shen, Lynn -- Turk, Erin -- Ouyang, Chensi -- Jacks, Tyler -- P30 CA014051/CA/NCI NIH HHS/ -- P30 CA014051-37/CA/NCI NIH HHS/ -- P30 CA014051-38/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Nov 5;462(7269):104-7. doi: 10.1038/nature08462. Epub 2009 Oct 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Koch Institute for Integrative Cancer Research, and Department of Biology, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19847165" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*metabolism/*pathology ; Animals ; Apoptosis ; Carcinoma, Non-Small-Cell Lung/metabolism/pathology ; Cell Line ; Cell Line, Tumor ; Cell Survival ; Cells, Cultured ; DNA/metabolism ; *Disease Models, Animal ; Fibroblasts ; Genes, p53/genetics ; Humans ; Lung Neoplasms/*metabolism/*pathology ; Mice ; NF-kappa B/antagonists & inhibitors/*metabolism ; Oncogene Protein p21(ras)/genetics/metabolism ; *Signal Transduction ; Transcription Factor RelA/metabolism ; Tumor Suppressor Protein p53/deficiency/genetics/metabolism
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    Clustering of InsP3 receptors by InsP3 retunes their regulation by InsP3 and Ca2+ (2009)
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    Publication Date: 2009-04-07
    Description: The versatility of Ca2+ signals derives from their spatio-temporal organization. For Ca2+ signals initiated by inositol-1,4,5-trisphosphate (InsP3), this requires local interactions between InsP3 receptors (InsP3Rs) mediated by their rapid stimulation and slower inhibition by cytosolic Ca2+. This allows hierarchical recruitment of Ca2+ release events as the InsP3 concentration increases. Single InsP3Rs respond first, then clustered InsP3Rs open together giving a local 'Ca2+ puff', and as puffs become more frequent they ignite regenerative Ca2+ waves. Using nuclear patch-clamp recording, here we demonstrate that InsP3Rs are initially randomly distributed with an estimated separation of 1 m. Low concentrations of InsP3 cause InsP3Rs to aggregate rapidly and reversibly into small clusters of about four closely associated InsP3Rs. At resting cytosolic [Ca2+], clustered InsP3Rs open independently, but with lower open probability, shorter open time, and less InsP3 sensitivity than lone InsP3Rs. Increasing cytosolic [Ca2+] reverses the inhibition caused by clustering, InsP3R gating becomes coupled, and the duration of multiple openings is prolonged. Clustering both exposes InsP3Rs to local Ca2+ rises and increases the effects of Ca2+. Dynamic regulation of clustering by InsP3 retunes InsP3R sensitivity to InsP3 and Ca2+, facilitating hierarchical recruitment of the elementary events that underlie all InsP3-evoked Ca2+ signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2702691/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2702691/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taufiq-Ur-Rahman -- Skupin, Alexander -- Falcke, Martin -- Taylor, Colin W -- 085295/Wellcome Trust/United Kingdom -- BBE0046601/Biotechnology and Biological Sciences Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2009 Apr 2;458(7238):655-9. doi: 10.1038/nature07763.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Tennis Court Road, Cambridge CB2 1PD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19348050" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; *Calcium Signaling ; Cell Line ; Cytosol/metabolism ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors/*metabolism ; Ion Channel Gating ; Patch-Clamp Techniques ; Protein Transport ; Rats
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    CtIP-BRCA1 modulates the choice of DNA double-strand-break repair pathway throughout the cell cycle (2009)
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    Publication Date: 2009-04-10
    Description: The repair of DNA double-strand breaks (DSBs) is tightly regulated during the cell cycle. In G1 phase, the absence of a sister chromatid means that repair of DSBs occurs through non-homologous end-joining or microhomology-mediated end-joining (MMEJ). These pathways often involve loss of DNA sequences at the break site and are therefore error-prone. In late S and G2 phases, even though DNA end-joining pathways remain functional, there is an increase in repair of DSBs by homologous recombination, which is mostly error-free. Consequently, the relative contribution of these different pathways to DSB repair in the cell cycle has a large influence on the maintenance of genetic integrity. It has remained unknown how DSBs are directed for repair by different, potentially competing, repair pathways. Here we identify a role for CtIP (also known as RBBP8) in this process in the avian B-cell line DT40. We establish that CtIP is required not only for repair of DSBs by homologous recombination in S/G2 phase but also for MMEJ in G1. The function of CtIP in homologous recombination, but not MMEJ, is dependent on the phosphorylation of serine residue 327 and recruitment of BRCA1. Cells expressing CtIP protein that cannot be phosphorylated at serine 327 are specifically defective in homologous recombination and have a decreased level of single-stranded DNA after DNA damage, whereas MMEJ remains unaffected. Our data support a model in which phosphorylation of serine 327 of CtIP as cells enter S phase and the recruitment of BRCA1 functions as a molecular switch to shift the balance of DSB repair from error-prone DNA end-joining to error-free homologous recombination.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2857324/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2857324/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yun, Maximina H -- Hiom, Kevin -- MC_U105184300/Medical Research Council/United Kingdom -- U.1051.03.005(78826)/Medical Research Council/United Kingdom -- England -- Nature. 2009 May 21;459(7245):460-3. doi: 10.1038/nature07955. Epub 2009 Apr 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Protein and Nucleic Acid Chemistry, MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19357644" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Proteins/*metabolism ; B-Lymphocytes/cytology/metabolism ; BRCA1 Protein/*metabolism ; Carrier Proteins/genetics/*metabolism ; *Cell Cycle ; Cell Line ; Chickens ; Cisplatin/pharmacology ; *DNA Breaks, Double-Stranded/radiation effects ; DNA Repair/genetics/*physiology ; G1 Phase ; G2 Phase ; Humans ; Nuclear Proteins/genetics/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Recombination, Genetic/genetics ; S Phase ; X-Rays
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    Cohesin acetylation speeds the replication fork (2009)
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    Publication Date: 2009-11-13
    Description: Cohesin not only links sister chromatids but also inhibits the transcriptional machinery's interaction with and movement along chromatin. In contrast, replication forks must traverse such cohesin-associated obstructions to duplicate the entire genome in S phase. How this occurs is unknown. Through single-molecule analysis, we demonstrate that the replication factor C (RFC)-CTF18 clamp loader (RFC(CTF18)) controls the velocity, spacing and restart activity of replication forks in human cells and is required for robust acetylation of cohesin's SMC3 subunit and sister chromatid cohesion. Unexpectedly, we discovered that cohesin acetylation itself is a central determinant of fork processivity, as slow-moving replication forks were found in cells lacking the Eco1-related acetyltransferases ESCO1 or ESCO2 (refs 8-10) (including those derived from Roberts' syndrome patients, in whom ESCO2 is biallelically mutated) and in cells expressing a form of SMC3 that cannot be acetylated. This defect was a consequence of cohesin's hyperstable interaction with two regulatory cofactors, WAPL and PDS5A (refs 12, 13); removal of either cofactor allowed forks to progress rapidly without ESCO1, ESCO2, or RFC(CTF18). Our results show a novel mechanism for clamp-loader-dependent fork progression, mediated by the post-translational modification and structural remodelling of the cohesin ring. Loss of this regulatory mechanism leads to the spontaneous accrual of DNA damage and may contribute to the abnormalities of the Roberts' syndrome cohesinopathy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777716/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777716/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Terret, Marie-Emilie -- Sherwood, Rebecca -- Rahman, Sadia -- Qin, Jun -- Jallepalli, Prasad V -- R01 CA107342/CA/NCI NIH HHS/ -- R01 CA107342-05/CA/NCI NIH HHS/ -- R01 GM094972/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Nov 12;462(7270):231-4. doi: 10.1038/nature08550.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19907496" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetyltransferases/deficiency/genetics ; Carrier Proteins/genetics/metabolism ; Cell Aging ; Cell Cycle Proteins/chemistry/*metabolism ; Cell Line ; Chromatids/metabolism ; Chromosomal Proteins, Non-Histone/chemistry/deficiency/genetics/*metabolism ; DNA Damage ; DNA Replication/drug effects/*physiology ; Humans ; Mutagens/toxicity ; Nuclear Proteins/genetics/metabolism ; Protein Subunits/metabolism ; Proto-Oncogene Proteins/metabolism ; Replication Protein C/metabolism
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    A newly discovered protein export machine in malaria parasites (2009)
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    Publication Date: 2009-06-19
    Description: Several hundred malaria parasite proteins are exported beyond an encasing vacuole and into the cytosol of the host erythrocyte, a process that is central to the virulence and viability of the causative Plasmodium species. The trafficking machinery responsible for this export is unknown. Here we identify in Plasmodium falciparum a translocon of exported proteins (PTEX), which is located in the vacuole membrane. The PTEX complex is ATP-powered, and comprises heat shock protein 101 (HSP101; a ClpA/B-like ATPase from the AAA+ superfamily, of a type commonly associated with protein translocons), a novel protein termed PTEX150 and a known parasite protein, exported protein 2 (EXP2). EXP2 is the potential channel, as it is the membrane-associated component of the core PTEX complex. Two other proteins, a new protein PTEX88 and thioredoxin 2 (TRX2), were also identified as PTEX components. As a common portal for numerous crucial processes, this translocon offers a new avenue for therapeutic intervention.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2725363/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2725363/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Koning-Ward, Tania F -- Gilson, Paul R -- Boddey, Justin A -- Rug, Melanie -- Smith, Brian J -- Papenfuss, Anthony T -- Sanders, Paul R -- Lundie, Rachel J -- Maier, Alexander G -- Cowman, Alan F -- Crabb, Brendan S -- R01 AI044008-11/AI/NIAID NIH HHS/ -- R01 AI44008/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jun 18;459(7249):945-9. doi: 10.1038/nature08104.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter & Eliza Hall Institute of Medical Research, Melbourne 3052, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19536257" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Malaria, Falciparum/*parasitology ; Models, Biological ; Multiprotein Complexes/*chemistry/*metabolism ; Plasmodium falciparum/*metabolism ; Protein Binding ; Protein Transport ; Protozoan Proteins/*metabolism
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    Global patterns of speciation and diversity (2009)
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    Publication Date: 2009-07-17
    Description: In recent years, strikingly consistent patterns of biodiversity have been identified over space, time, organism type and geographical region. A neutral theory (assuming no environmental selection or organismal interactions) has been shown to predict many patterns of ecological biodiversity. This theory is based on a mechanism by which new species arise similarly to point mutations in a population without sexual reproduction. Here we report the simulation of populations with sexual reproduction, mutation and dispersal. We found simulated time dependence of speciation rates, species-area relationships and species abundance distributions consistent with the behaviours found in nature. From our results, we predict steady speciation rates, more species in one-dimensional environments than two-dimensional environments, three scaling regimes of species-area relationships and lognormal distributions of species abundance with an excess of rare species and a tail that may be approximated by Fisher's logarithmic series. These are consistent with dependences reported for, among others, global birds and flowering plants, marine invertebrate fossils, ray-finned fishes, British birds and moths, North American songbirds, mammal fossils from Kansas and Panamanian shrubs. Quantitative comparisons of specific cases are remarkably successful. Our biodiversity results provide additional evidence that species diversity arises without specific physical barriers. This is similar to heavy traffic flows, where traffic jams can form even without accidents or barriers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Aguiar, M A M -- Baranger, M -- Baptestini, E M -- Kaufman, L -- Bar-Yam, Y -- England -- Nature. 2009 Jul 16;460(7253):384-7. doi: 10.1038/nature08168.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉New England Complex Systems Institute, Cambridge, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19606148" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; Disorders of Sex Development ; Extinction, Biological ; *Genetic Speciation ; Genotype ; Haploidy ; Models, Biological ; Mutation/genetics ; Population Dynamics ; Reproduction/genetics/*physiology ; Sexual Behavior, Animal ; Time Factors
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    DNA demethylation in hormone-induced transcriptional derepression (2009)
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    Publication Date: 2009-10-16
    Description: Epigenetic modifications at the histone level affect gene regulation in response to extracellular signals. However, regulated epigenetic modifications at the DNA level, especially active DNA demethylation, in gene activation are not well understood. Here we report that DNA methylation/demethylation is hormonally switched to control transcription of the cytochrome p450 27B1 (CYP27B1) gene. Reflecting vitamin-D-mediated transrepression of the CYP27B1 gene by the negative vitamin D response element (nVDRE), methylation of CpG sites ((5m)CpG) is induced by vitamin D in this gene promoter. Conversely, treatment with parathyroid hormone, a hormone known to activate the CYP27B1 gene, induces active demethylation of the (5m)CpG sites in this promoter. Biochemical purification of a complex associated with the nVDRE-binding protein (VDIR, also known as TCF3) identified two DNA methyltransferases, DNMT1 and DNMT3B, for methylation of CpG sites, as well as a DNA glycosylase, MBD4 (ref. 10). Protein-kinase-C-phosphorylated MBD4 by parathyroid hormone stimulation promotes incision of methylated DNA through glycosylase activity, and a base-excision repair process seems to complete DNA demethylation in the MBD4-bound promoter. Such parathyroid-hormone-induced DNA demethylation and subsequent transcriptional derepression are impaired in Mbd4(-/-) mice. Thus, the present findings suggest that methylation switching at the DNA level contributes to the hormonal control of transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Mi-Sun -- Kondo, Takeshi -- Takada, Ichiro -- Youn, Min-Young -- Yamamoto, Yoko -- Takahashi, Sayuri -- Matsumoto, Takahiro -- Fujiyama, Sally -- Shirode, Yuko -- Yamaoka, Ikuko -- Kitagawa, Hirochika -- Takeyama, Ken-ichi -- Shibuya, Hiroshi -- Ohtake, Fumiaki -- Kato, Shigeaki -- England -- Nature. 2009 Oct 15;461(7266):1007-12. doi: 10.1038/nature08456.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ERATO, Japan Science and Technology Agency, 4-1-8 Honcho, Kawaguchisi, Saitama 332-0012, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19829383" target="_blank"〉PubMed〈/a〉
    Keywords: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase/genetics ; Animals ; Cell Line ; CpG Islands/genetics ; DNA (Cytosine-5-)-Methyltransferase/metabolism ; DNA Glycosylases/metabolism ; DNA Methylation/*drug effects ; Down-Regulation/drug effects ; Endodeoxyribonucleases/deficiency/genetics ; Mice ; Parathyroid Hormone/*pharmacology ; Phosphorylation ; Protein Kinase C/metabolism ; Response Elements/genetics ; Transcription, Genetic/*drug effects ; Vitamin D/pharmacology
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    We must reverse the Bush legacy of stem-cell problems (2009)
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    Publication Date: 2009-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas Scott, Christopher -- Owen-Smith, Jason -- McCormick, Jennifer -- England -- Nature. 2009 Jul 2;460(7251):33. doi: 10.1038/460033b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19571864" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Federal Government ; *Guidelines as Topic ; Humans ; *National Institutes of Health (U.S.) ; *Stem Cells ; United States
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    Multiple roles for MRE11 at uncapped telomeres (2009)
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    Publication Date: 2009-07-28
    Description: Progressive telomere attrition or uncapping of the shelterin complex elicits a DNA damage response as a result of a cell's inability to distinguish dysfunctional telomeric ends from DNA double-strand breaks. Telomere deprotection activates both ataxia telangiectasia mutated (ATM) and telangiectasia and Rad3-related (ATR) kinase-dependent DNA damage response pathways, and promotes efficient non-homologous end-joining (NHEJ) of dysfunctional telomeres. The mammalian MRE11-RAD50-NBS1 (MRN; NBS1 is also known as NBN) complex interacts with ATM to sense chromosomal double-strand breaks and coordinate global DNA damage responses. Although the MRN complex accumulates at dysfunctional telomeres, it is not known whether mammalian MRN promotes repair at these sites. Here we address this question by using mouse alleles that either inactivate the entire MRN complex or eliminate only the nuclease activities of MRE11 (ref. 8). We show that cells lacking MRN do not activate ATM when telomeric repeat binding factor 2 (TRF2) is removed from telomeres, and ligase 4 (LIG4)-dependent chromosome end-to-end fusions are markedly reduced. Residual chromatid fusions involve only telomeres generated by leading strand synthesis. Notably, although cells deficient for MRE11 nuclease activity efficiently activate ATM and recruit 53BP1 (also known as TP53BP1) to deprotected telomeres, the 3' telomeric overhang persists to prevent NHEJ-mediated chromosomal fusions. Removal of shelterin proteins that protect the 3' overhang in the setting of MRE11 nuclease deficiency restores LIG4-dependent chromosome fusions. Our data indicate a critical role for the MRN complex in sensing dysfunctional telomeres, and show that in the absence of TRF2, MRE11 nuclease activity removes the 3' telomeric overhang to promote chromosome fusions. MRE11 can also protect newly replicated leading strand telomeres from NHEJ by promoting 5' strand resection to generate POT1a-TPP1-bound 3' overhangs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2760383/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2760383/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deng, Yibin -- Guo, Xiaolan -- Ferguson, David O -- Chang, Sandy -- K01CA124461/CA/NCI NIH HHS/ -- P30 CA046592/CA/NCI NIH HHS/ -- R01 AG028888/AG/NIA NIH HHS/ -- R01 AG028888-02/AG/NIA NIH HHS/ -- R01 CA129037/CA/NCI NIH HHS/ -- R01 CA129037-02/CA/NCI NIH HHS/ -- R01 HL079118/HL/NHLBI NIH HHS/ -- England -- Nature. 2009 Aug 13;460(7257):914-8. doi: 10.1038/nature08196. Epub 2009 Jul 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Box 1010, The M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19633651" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/genetics/metabolism ; Alleles ; Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/genetics/metabolism ; Cell Line ; Chromosomal Proteins, Non-Histone ; Chromosome Aberrations ; DNA Damage ; DNA Ligases/metabolism ; DNA Repair Enzymes/deficiency/genetics/*metabolism ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Fibroblasts ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice ; Nuclear Proteins/deficiency/genetics/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Telomere/genetics/*metabolism ; Telomeric Repeat Binding Protein 2/deficiency/metabolism ; Tumor Suppressor Proteins/metabolism
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    Journal club. A cell biologist looks at the risk and promise of a new insight into stem cells and cancer (2009)
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    Publication Date: 2009-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knoepfler, Paul -- England -- Nature. 2009 Jan 22;457(7228):361. doi: 10.1038/457361e.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California, Davis, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19158746" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Comparative Genomic Hybridization ; Embryonic Stem Cells/*cytology/*pathology ; Humans ; Neoplasms/*pathology ; Neoplastic Stem Cells/pathology ; Pluripotent Stem Cells/*cytology/*pathology
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    A tunable synthetic mammalian oscillator (2009)
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    Publication Date: 2009-01-17
    Description: Autonomous and self-sustained oscillator circuits mediating the periodic induction of specific target genes are minimal genetic time-keeping devices found in the central and peripheral circadian clocks. They have attracted significant attention because of their intriguing dynamics and their importance in controlling critical repair, metabolic and signalling pathways. The precise molecular mechanism and expression dynamics of this mammalian circadian clock are still not fully understood. Here we describe a synthetic mammalian oscillator based on an auto-regulated sense-antisense transcription control circuit encoding a positive and a time-delayed negative feedback loop, enabling autonomous, self-sustained and tunable oscillatory gene expression. After detailed systems design with experimental analyses and mathematical modelling, we monitored oscillating concentrations of green fluorescent protein with tunable frequency and amplitude by time-lapse microscopy in real time in individual Chinese hamster ovary cells. The synthetic mammalian clock may provide an insight into the dynamics of natural periodic processes and foster advances in the design of prosthetic networks in future gene and cell therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tigges, Marcel -- Marquez-Lago, Tatiana T -- Stelling, Jorg -- Fussenegger, Martin -- England -- Nature. 2009 Jan 15;457(7227):309-12. doi: 10.1038/nature07616.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biosystems Science and Engineering, ETH Zurich, Mattenstrasse 26, CH-4058 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19148099" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/*physiology ; CHO Cells ; Circadian Rhythm/*physiology ; Cricetinae ; Cricetulus ; Feedback, Physiological ; Fluorescence ; Gene Expression Regulation/*genetics ; Genes, Synthetic/*genetics ; *Genetic Engineering ; Green Fluorescent Proteins/analysis/genetics/metabolism ; Models, Biological ; Reproducibility of Results ; Time Factors ; Transcription, Genetic
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    iPS cells produce viable mice through tetraploid complementation (2009)
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    Publication Date: 2009-08-13
    Description: Since the initial description of induced pluripotent stem (iPS) cells created by forced expression of four transcription factors in mouse fibroblasts, the technique has been used to generate embryonic stem (ES)-cell-like pluripotent cells from a variety of cell types in other species, including primates and rat. It has become a popular means to reprogram somatic genomes into an embryonic-like pluripotent state, and a preferred alternative to somatic-cell nuclear transfer and somatic-cell fusion with ES cells. However, iPS cell reprogramming remains slow and inefficient. Notably, no live animals have been produced by the most stringent tetraploid complementation assay, indicative of a failure to create fully pluripotent cells. Here we report the generation of several iPS cell lines that are capable of generating viable, fertile live-born progeny by tetraploid complementation. These iPS cells maintain a pluripotent potential that is very close to ES cells generated from in vivo or nuclear transfer embryos. We demonstrate the practicality of using iPS cells as useful tools for the characterization of cellular reprogramming and developmental potency, and confirm that iPS cells can attain true pluripotency that is similar to that of ES cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Xiao-yang -- Li, Wei -- Lv, Zhuo -- Liu, Lei -- Tong, Man -- Hai, Tang -- Hao, Jie -- Guo, Chang-long -- Ma, Qing-wen -- Wang, Liu -- Zeng, Fanyi -- Zhou, Qi -- England -- Nature. 2009 Sep 3;461(7260):86-90. doi: 10.1038/nature08267.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19672241" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/cytology/physiology ; Cell Dedifferentiation/physiology ; Cell Line ; Cell Lineage ; Cellular Reprogramming ; Embryo, Mammalian/cytology/embryology/metabolism ; Embryonic Stem Cells/cytology/physiology ; Female ; Fibroblasts/cytology ; Gene Expression Profiling ; Genetic Complementation Test ; Male ; Mice ; Mice, SCID ; Pluripotent Stem Cells/cytology/*physiology ; *Polyploidy ; Pregnancy ; *Reproductive Techniques ; Survival Rate ; Teratoma
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    Global Darwin: Contempt for competition (2009)
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    Publication Date: 2009-11-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Todes, Daniel -- England -- Nature. 2009 Nov 5;462(7269):36-7. doi: 10.1038/462036a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of the History of Medicine at Johns Hopkins University, 1900 East Monument Street, Baltimore, Maryland 21205, USA. dtodes@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19890312" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Biological Science Disciplines/*history ; *Competitive Behavior ; Cooperative Behavior ; *Cultural Diversity ; Food Supply ; Great Britain ; History, 19th Century ; History, 20th Century ; Humans ; Literature, Modern/history ; Metaphor ; Models, Biological ; Population Density ; Russia ; Selection, Genetic
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    Cohesins form chromosomal cis-interactions at the developmentally regulated IFNG locus (2009)
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    Publication Date: 2009-05-22
    Description: Cohesin-mediated sister chromatid cohesion is essential for chromosome segregation and post-replicative DNA repair. In addition, evidence from model organisms and from human genetics suggests that cohesin is involved in the control of gene expression. This non-canonical role has recently been rationalized by the findings that mammalian cohesin complexes are recruited to a subset of DNase I hypersensitive sites and to conserved noncoding sequences by the DNA-binding protein CTCF. CTCF functions at insulators (which control interactions between enhancers and promoters) and at boundary elements (which demarcate regions of distinct chromatin structure), and cohesin contributes to its enhancer-blocking activity. The underlying mechanisms remain unknown, and the full spectrum of cohesin functions remains to be determined. Here we show that cohesin forms the topological and mechanistic basis for cell-type-specific long-range chromosomal interactions in cis at the developmentally regulated cytokine locus IFNG. Hence, the ability of cohesin to constrain chromosome topology is used not only for the purpose of sister chromatid cohesion, but also to dynamically define the spatial conformation of specific loci. This new aspect of cohesin function is probably important for normal development and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2869028/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2869028/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hadjur, Suzana -- Williams, Luke M -- Ryan, Natalie K -- Cobb, Bradley S -- Sexton, Tom -- Fraser, Peter -- Fisher, Amanda G -- Merkenschlager, Matthias -- G0900491/Medical Research Council/United Kingdom -- G117/530/Medical Research Council/United Kingdom -- MC_U120027516/Medical Research Council/United Kingdom -- U.1200(U.1200)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2009 Jul 16;460(7253):410-3. doi: 10.1038/nature08079. Epub 2009 May 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Development Group, MRC Clinical Sciences Centre, Imperial College London, Du Cane Road, London W12 0NN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19458616" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/metabolism ; Cell Cycle Proteins/*metabolism ; Cell Line ; Chromosomal Proteins, Non-Histone/*metabolism ; Chromosomes/*genetics/*metabolism ; *Gene Expression Regulation, Developmental ; Histones/metabolism ; Humans ; Interferon-gamma/*genetics ; Mice ; Nuclear Proteins/genetics/metabolism ; Organ Specificity ; Phosphoproteins/genetics/metabolism ; Repressor Proteins/metabolism
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    Human-specific transcriptional regulation of CNS development genes by FOXP2 (2009)
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    Publication Date: 2009-11-13
    Description: The signalling pathways controlling both the evolution and development of language in the human brain remain unknown. So far, the transcription factor FOXP2 (forkhead box P2) is the only gene implicated in Mendelian forms of human speech and language dysfunction. It has been proposed that the amino acid composition in the human variant of FOXP2 has undergone accelerated evolution, and this two-amino-acid change occurred around the time of language emergence in humans. However, this remains controversial, and whether the acquisition of these amino acids in human FOXP2 has any functional consequence in human neurons remains untested. Here we demonstrate that these two human-specific amino acids alter FOXP2 function by conferring differential transcriptional regulation in vitro. We extend these observations in vivo to human and chimpanzee brain, and use network analysis to identify novel relationships among the differentially expressed genes. These data provide experimental support for the functional relevance of changes in FOXP2 that occur on the human lineage, highlighting specific pathways with direct consequences for human brain development and disease in the central nervous system (CNS). Because FOXP2 has an important role in speech and language in humans, the identified targets may have a critical function in the development and evolution of language circuitry in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778075/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778075/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Konopka, Genevieve -- Bomar, Jamee M -- Winden, Kellen -- Coppola, Giovanni -- Jonsson, Zophonias O -- Gao, Fuying -- Peng, Sophia -- Preuss, Todd M -- Wohlschlegel, James A -- Geschwind, Daniel H -- N01-HD-4-3368/HD/NICHD NIH HHS/ -- N01-HD-4-3383/HD/NICHD NIH HHS/ -- R21 MH075028/MH/NIMH NIH HHS/ -- R21 MH075028-02/MH/NIMH NIH HHS/ -- R21MH075028/MH/NIMH NIH HHS/ -- R37 MH060233/MH/NIMH NIH HHS/ -- R37 MH060233-06A1/MH/NIMH NIH HHS/ -- R37MH60233-06A1/MH/NIMH NIH HHS/ -- RR00165/RR/NCRR NIH HHS/ -- T32HD007032/HD/NICHD NIH HHS/ -- T32MH073526/MH/NIMH NIH HHS/ -- England -- Nature. 2009 Nov 12;462(7270):213-7. doi: 10.1038/nature08549.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Neurogenetics, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA. gena@alum.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19907493" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/*embryology/*metabolism ; Cell Line ; Evolution, Molecular ; Forkhead Transcription Factors/chemistry/genetics/*metabolism ; *Gene Expression Regulation, Developmental ; Humans ; Language ; Pan troglodytes/embryology/genetics/metabolism ; Promoter Regions, Genetic/genetics ; Species Specificity ; Speech/physiology ; *Transcription, Genetic ; Transcriptional Activation
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    A regulatory circuit for piwi by the large Maf gene traffic jam in Drosophila (2009)
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    Publication Date: 2009-10-09
    Description: PIWI-interacting RNAs (piRNAs) silence retrotransposons in Drosophila germ lines by associating with the PIWI proteins Argonaute 3 (AGO3), Aubergine (Aub) and Piwi. piRNAs in Drosophila are produced from intergenic repetitive genes and piRNA clusters by two systems: the primary processing pathway and the amplification loop. The amplification loop occurs in a Dicer-independent, PIWI-Slicer-dependent manner. However, primary piRNA processing remains elusive. Here we analysed piRNA processing in a Drosophila ovarian somatic cell line where Piwi, but not Aub or AGO3, is expressed; thus, only the primary piRNAs exist. In addition to flamenco, a Piwi-specific piRNA cluster, traffic jam (tj), a large Maf gene, was determined as a new piRNA cluster. piRNAs arising from tj correspond to the untranslated regions of tj messenger RNA and are sense-oriented. piRNA loading on to Piwi may occur in the cytoplasm. zucchini, a gene encoding a putative cytoplasmic nuclease, is required for tj-derived piRNA production. In tj and piwi mutant ovaries, somatic cells fail to intermingle with germ cells and Fasciclin III is overexpressed. Loss of tj abolishes Piwi expression in gonadal somatic cells. Thus, in gonadal somatic cells, tj gives rise simultaneously to two different molecules: the TJ protein, which activates Piwi expression, and piRNAs, which define the Piwi targets for silencing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saito, Kuniaki -- Inagaki, Sachi -- Mituyama, Toutai -- Kawamura, Yoshinori -- Ono, Yukiteru -- Sakota, Eri -- Kotani, Hazuki -- Asai, Kiyoshi -- Siomi, Haruhiko -- Siomi, Mikiko C -- England -- Nature. 2009 Oct 29;461(7268):1296-9. doi: 10.1038/nature08501. Epub 2009 Oct 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Keio University School of Medicine, Tokyo 160-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19812547" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; Cell Adhesion Molecules, Neuronal/metabolism ; Cell Line ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/genetics/*metabolism ; Endoribonucleases/metabolism ; Female ; Genes, Insect/genetics ; Genetic Loci/genetics ; Maf Transcription Factors, Large/genetics/*metabolism ; Male ; Ovary/cytology/metabolism ; Phenotype ; Proto-Oncogene Proteins/genetics/*metabolism ; RNA/biosynthesis/genetics/*metabolism ; RNA Interference ; RNA Processing, Post-Transcriptional ; RNA-Induced Silencing Complex/genetics/*metabolism ; Testis/cytology/metabolism
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    Kinetochore geometry defined by cohesion within the centromere (2009)
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    Publication Date: 2009-04-17
    Description: During cell division microtubules capture chromosomes by binding to the kinetochore assembled in the centromeric region of chromosomes. In mitosis sister chromatids are captured by microtubules emanating from both spindle poles, a process called bipolar attachment, whereas in meiosis I sisters are attached to microtubules originating from one spindle pole, called monopolar attachment. For determining chromosome orientation, kinetochore geometry or structure might be an important target of regulation. However, the molecular basis of this regulation has remained elusive. Here we show the link between kinetochore orientation and cohesion within the centromere in fission yeast Schizosaccharomyces pombe by strategies developed to visualize the concealed cohesion within the centromere, and to introduce artificial tethers that can influence kinetochore geometry. Our data imply that cohesion at the core centromere induces the mono-orientation of kinetochores whereas cohesion at the peri-centromeric region promotes bi-orientation. Our study may reveal a general mechanism for the geometric regulation of kinetochores, which collaborates with previously defined tension-dependent reorientation machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sakuno, Takeshi -- Tada, Kenji -- Watanabe, Yoshinori -- England -- Nature. 2009 Apr 16;458(7240):852-8. doi: 10.1038/nature07876.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19370027" target="_blank"〉PubMed〈/a〉
    Keywords: Centromere/genetics/*metabolism ; Chromosome Segregation ; Kinetochores/*metabolism ; Meiosis ; Microtubules/metabolism ; Mitosis ; Models, Biological ; Schizosaccharomyces/*cytology
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    The SUMO modification pathway is involved in the BRCA1 response to genotoxic stress (2009)
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    Publication Date: 2009-12-18
    Description: Mutations in BRCA1 are associated with a high risk of breast and ovarian cancer. BRCA1 participates in the DNA damage response and acts as a ubiquitin ligase. However, its regulation remains poorly understood. Here we report that BRCA1 is modified by small ubiquitin-like modifier (SUMO) in response to genotoxic stress, and co-localizes at sites of DNA damage with SUMO1, SUMO2/3 and the SUMO-conjugating enzyme Ubc9. PIAS SUMO E3 ligases co-localize with and modulate SUMO modification of BRCA1, and are required for BRCA1 ubiquitin ligase activity in cells. In vitro SUMO modification of the BRCA1/BARD1 heterodimer greatly increases its ligase activity, identifying it as a SUMO-regulated ubiquitin ligase (SRUbL). Further, PIAS SUMO ligases are required for complete accumulation of double-stranded DNA (dsDNA) damage-repair proteins subsequent to RNF8 accrual, and for proficient double-strand break repair. These data demonstrate that the SUMOylation pathway plays a significant role in mammalian DNA damage response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morris, Joanna R -- Boutell, Chris -- Keppler, Melanie -- Densham, Ruth -- Weekes, Daniel -- Alamshah, Amin -- Butler, Laura -- Galanty, Yaron -- Pangon, Laurent -- Kiuchi, Tai -- Ng, Tony -- Solomon, Ellen -- 10331/Cancer Research UK/United Kingdom -- 6900577/Medical Research Council/United Kingdom -- C8820/A9494/Cancer Research UK/United Kingdom -- G0100152 #56891/Medical Research Council/United Kingdom -- G9600577/Medical Research Council/United Kingdom -- MC_UP_A550_1030/Medical Research Council/United Kingdom -- England -- Nature. 2009 Dec 17;462(7275):886-90. doi: 10.1038/nature08593.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical and Molecular Genetics, King's College London, Guy's Medical School Campus, London SE1 9RT, UK. jo.morris@genetics.kcl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016594" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/*metabolism ; COS Cells ; Cell Line ; Cercopithecus aethiops ; DNA Breaks, Double-Stranded ; *DNA Damage ; DNA Repair ; HeLa Cells ; Histones/metabolism ; Humans ; Protein Inhibitors of Activated STAT/metabolism ; Small Ubiquitin-Related Modifier Proteins/*metabolism ; Ubiquitin-Conjugating Enzymes/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination
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    Antiviral immunity in Drosophila requires systemic RNA interference spread (2009)
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    Publication Date: 2009-02-11
    Description: Multicellular organisms evolved sophisticated defence systems to confer protection against pathogens. An important characteristic of these immune systems is their ability to act both locally at the site of infection and at distal uninfected locations. In insects, such as Drosophila melanogaster, RNA interference (RNAi) mediates antiviral immunity. However, the antiviral RNAi defence in flies seems to be a local, cell-autonomous process, as flies are thought to be unable to generate a systemic RNAi response. Here we show that a recently defined double-stranded RNA (dsRNA) uptake pathway is essential for effective antiviral RNAi immunity in adult flies. Mutant flies defective in this dsRNA uptake pathway were hypersensitive to infection with Drosophila C virus and Sindbis virus. Mortality in dsRNA-uptake-defective flies was accompanied by 100-to 10(5)-fold increases in viral titres and higher levels of viral RNA. Furthermore, inoculating naked dsRNA into flies elicited a sequence-specific antiviral immune response that required an intact dsRNA uptake pathway. These findings suggest that spread of dsRNA to uninfected sites is essential for effective antiviral immunity. Notably, infection with green fluorescent protein (GFP)-tagged Sindbis virus suppressed expression of host-encoded GFP at a distal site. Thus, similar to protein-based immunity in vertebrates, the antiviral RNAi response in flies also relies on the systemic spread of a virus-specific immunity signal.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978076/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978076/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saleh, Maria-Carla -- Tassetto, Michel -- van Rij, Ronald P -- Goic, Bertsy -- Gausson, Valerie -- Berry, Bassam -- Jacquier, Caroline -- Antoniewski, Christophe -- Andino, Raul -- AI064738/AI/NIAID NIH HHS/ -- AI40085/AI/NIAID NIH HHS/ -- R01 AI040085/AI/NIAID NIH HHS/ -- R01 AI064738/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Mar 19;458(7236):346-50. doi: 10.1038/nature07712. Epub 2009 Feb 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California, San Francisco 94122-2280, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19204732" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Drosophila melanogaster/genetics/*immunology/microbiology/*virology ; Micrococcus luteus/immunology ; Pectobacterium carotovorum/immunology ; RNA Interference/*immunology ; RNA Viruses/*immunology/physiology ; RNA, Double-Stranded/genetics/immunology/metabolism ; Sindbis Virus/genetics/growth & development/immunology ; Substrate Specificity
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    Molecular biology: Concealed enzyme coordination (2009)
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    Publication Date: 2009-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbondanzieri, Elio A -- Zhuang, Xiaowei -- England -- Nature. 2009 Jan 22;457(7228):392-3. doi: 10.1038/457392a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19158782" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/*chemistry/*metabolism ; Bacillus Phages/*enzymology ; DNA, Viral/chemistry/metabolism ; Hydrolysis ; Models, Biological ; Protein Structure, Quaternary ; Protein Subunits/chemistry/metabolism ; Virus Assembly
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    The pluripotency factor Oct4 interacts with Ctcf and also controls X-chromosome pairing and counting (2009)
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    Publication Date: 2009-06-19
    Description: Pluripotency of embryonic stem (ES) cells is controlled by defined transcription factors. During differentiation, mouse ES cells undergo global epigenetic reprogramming, as exemplified by X-chromosome inactivation (XCI) in which one female X chromosome is silenced to achieve gene dosage parity between the sexes. Somatic XCI is regulated by homologous X-chromosome pairing and counting, and by the random choice of future active and inactive X chromosomes. XCI and cell differentiation are tightly coupled, as blocking one process compromises the other and dedifferentiation of somatic cells to induced pluripotent stem cells is accompanied by X chromosome reactivation. Recent evidence suggests coupling of Xist expression to pluripotency factors occurs, but how the two are interconnected remains unknown. Here we show that Oct4 (also known as Pou5f1) lies at the top of the XCI hierarchy, and regulates XCI by triggering X-chromosome pairing and counting. Oct4 directly binds Tsix and Xite, two regulatory noncoding RNA genes of the X-inactivation centre, and also complexes with XCI trans-factors, Ctcf and Yy1 (ref. 17), through protein-protein interactions. Depletion of Oct4 blocks homologous X-chromosome pairing and results in the inactivation of both X chromosomes in female cells. Thus, we have identified the first trans-factor that regulates counting, and ascribed new functions to Oct4 during X-chromosome reprogramming.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057664/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057664/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Donohoe, Mary E -- Silva, Susana S -- Pinter, Stefan F -- Xu, Na -- Lee, Jeannie T -- GM58839/GM/NIGMS NIH HHS/ -- R01 GM058839/GM/NIGMS NIH HHS/ -- R01 GM058839-10/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jul 2;460(7251):128-32. doi: 10.1038/nature08098. Epub 2009 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19536159" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Chromosome Pairing ; Female ; Humans ; Male ; Mice ; Octamer Transcription Factor-3/deficiency/genetics/*metabolism ; Protein Binding ; RNA, Long Noncoding ; RNA, Untranslated/genetics ; Repressor Proteins/*metabolism ; SOXB1 Transcription Factors ; Transcriptional Activation ; X Chromosome/*genetics/*metabolism ; X Chromosome Inactivation/*genetics ; YY1 Transcription Factor/metabolism
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    Detection and trapping of intermediate states priming nicotinic receptor channel opening (2009)
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    Publication Date: 2009-04-03
    Description: In the course of synaptic transmission in the brain and periphery, acetylcholine receptors (AChRs) rapidly transduce a chemical signal into an electrical impulse. The speed of transduction is facilitated by rapid ACh association and dissociation, suggesting a binding site relatively non-selective for small cations. Selective transduction has been thought to originate from the ability of ACh, over that of other organic cations, to trigger the subsequent channel-opening step. However, transitions to and from the open state were shown to be similar for agonists with widely different efficacies. By studying mutant AChRs, we show here that the ultimate closed-to-open transition is agonist-independent and preceded by two primed closed states; the first primed state elicits brief openings, whereas the second elicits long-lived openings. Long-lived openings and the associated primed state are detected in the absence and presence of an agonist, and exhibit the same kinetic signatures under both conditions. By covalently locking the agonist-binding sites in the bound conformation, we find that each site initiates a priming step. Thus, a change in binding-site conformation primes the AChR for channel opening in a process that enables selective activation by ACh while maximizing the speed and efficiency of the biological response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712348/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712348/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mukhtasimova, Nuriya -- Lee, Won Yong -- Wang, Hai-Long -- Sine, Steven M -- NS031744/NS/NINDS NIH HHS/ -- R01 NS031744/NS/NINDS NIH HHS/ -- R01 NS031744-18/NS/NINDS NIH HHS/ -- England -- Nature. 2009 May 21;459(7245):451-4. doi: 10.1038/nature07923. Epub 2009 Apr 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Receptor Biology Laboratory, Department of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19339970" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Disulfides/metabolism ; Electric Conductivity ; Humans ; Kinetics ; Models, Molecular ; *Movement ; Nicotinic Agonists/pharmacology ; Patch-Clamp Techniques ; Protein Structure, Tertiary ; Receptors, Nicotinic/*chemistry/genetics/*metabolism ; Synaptic Transmission/physiology ; Torpedo
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    Carbon cycle: Sink in the African jungle (2009)
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    Publication Date: 2009-02-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller-Landau, Helene C -- England -- Nature. 2009 Feb 19;457(7232):969-70. doi: 10.1038/457969a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19225510" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Atmosphere/chemistry ; Biomass ; Carbon/analysis/*metabolism ; Carbon Dioxide/analysis/metabolism ; Models, Biological ; Trees/chemistry/growth & development/*metabolism ; *Tropical Climate ; Wilderness
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    NAADP mobilizes calcium from acidic organelles through two-pore channels (2009)
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    Publication Date: 2009-04-24
    Description: Ca(2+) mobilization from intracellular stores represents an important cell signalling process that is regulated, in mammalian cells, by inositol-1,4,5-trisphosphate (InsP(3)), cyclic ADP ribose and nicotinic acid adenine dinucleotide phosphate (NAADP). InsP(3) and cyclic ADP ribose cause the release of Ca(2+) from sarcoplasmic/endoplasmic reticulum stores by the activation of InsP(3) and ryanodine receptors (InsP(3)Rs and RyRs). In contrast, the nature of the intracellular stores targeted by NAADP and the molecular identity of the NAADP receptors remain controversial, although evidence indicates that NAADP mobilizes Ca(2+) from lysosome-related acidic compartments. Here we show that two-pore channels (TPCs) comprise a family of NAADP receptors, with human TPC1 (also known as TPCN1) and chicken TPC3 (TPCN3) being expressed on endosomal membranes, and human TPC2 (TPCN2) on lysosomal membranes when expressed in HEK293 cells. Membranes enriched with TPC2 show high affinity NAADP binding, and TPC2 underpins NAADP-induced Ca(2+) release from lysosome-related stores that is subsequently amplified by Ca(2+)-induced Ca(2+) release by InsP(3)Rs. Responses to NAADP were abolished by disrupting the lysosomal proton gradient and by ablating TPC2 expression, but were only attenuated by depleting endoplasmic reticulum Ca(2+) stores or by blocking InsP(3)Rs. Thus, TPCs form NAADP receptors that release Ca(2+) from acidic organelles, which can trigger further Ca(2+) signals via sarcoplasmic/endoplasmic reticulum. TPCs therefore provide new insights into the regulation and organization of Ca(2+) signals in animal cells, and will advance our understanding of the physiological role of NAADP.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2761823/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2761823/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Calcraft, Peter J -- Ruas, Margarida -- Pan, Zui -- Cheng, Xiaotong -- Arredouani, Abdelilah -- Hao, Xuemei -- Tang, Jisen -- Rietdorf, Katja -- Teboul, Lydia -- Chuang, Kai-Ting -- Lin, Peihui -- Xiao, Rui -- Wang, Chunbo -- Zhu, Yingmin -- Lin, Yakang -- Wyatt, Christopher N -- Parrington, John -- Ma, Jianjie -- Evans, A Mark -- Galione, Antony -- Zhu, Michael X -- 070772/Wellcome Trust/United Kingdom -- FS/05/050/British Heart Foundation/United Kingdom -- P30 NS045758/NS/NINDS NIH HHS/ -- P30 NS045758-05/NS/NINDS NIH HHS/ -- P30 NS045758-059003/NS/NINDS NIH HHS/ -- P30-NS045758/NS/NINDS NIH HHS/ -- R01 DK081654/DK/NIDDK NIH HHS/ -- R01 DK081654-01A1/DK/NIDDK NIH HHS/ -- R01 NS042183/NS/NINDS NIH HHS/ -- R01 NS042183-04/NS/NINDS NIH HHS/ -- R21 NS056942/NS/NINDS NIH HHS/ -- R21 NS056942-01/NS/NINDS NIH HHS/ -- England -- Nature. 2009 May 28;459(7246):596-600. doi: 10.1038/nature08030. Epub 2009 Apr 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Integrative Physiology, College of Medicine and Veterinary Medicine, University of Edinburgh, Hugh Robson Building, Edinburgh EH8 9XD, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19387438" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/genetics/*metabolism ; *Calcium Signaling/drug effects ; Cell Line ; Chickens ; Humans ; Hydrogen-Ion Concentration ; Insulin-Secreting Cells/drug effects/metabolism ; Mice ; Mice, Knockout ; Molecular Sequence Data ; NADP/*analogs & derivatives/metabolism/pharmacology ; Organelles/drug effects/*metabolism ; Protein Binding
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    AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity (2009)
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    Publication Date: 2009-03-06
    Description: AMP-activated protein kinase (AMPK) is a metabolic fuel gauge conserved along the evolutionary scale in eukaryotes that senses changes in the intracellular AMP/ATP ratio. Recent evidence indicated an important role for AMPK in the therapeutic benefits of metformin, thiazolidinediones and exercise, which form the cornerstones of the clinical management of type 2 diabetes and associated metabolic disorders. In general, activation of AMPK acts to maintain cellular energy stores, switching on catabolic pathways that produce ATP, mostly by enhancing oxidative metabolism and mitochondrial biogenesis, while switching off anabolic pathways that consume ATP. This regulation can take place acutely, through the regulation of fast post-translational events, but also by transcriptionally reprogramming the cell to meet energetic needs. Here we demonstrate that AMPK controls the expression of genes involved in energy metabolism in mouse skeletal muscle by acting in coordination with another metabolic sensor, the NAD+-dependent type III deacetylase SIRT1. AMPK enhances SIRT1 activity by increasing cellular NAD+ levels, resulting in the deacetylation and modulation of the activity of downstream SIRT1 targets that include the peroxisome proliferator-activated receptor-gamma coactivator 1alpha and the forkhead box O1 (FOXO1) and O3 (FOXO3a) transcription factors. The AMPK-induced SIRT1-mediated deacetylation of these targets explains many of the convergent biological effects of AMPK and SIRT1 on energy metabolism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616311/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616311/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Canto, Carles -- Gerhart-Hines, Zachary -- Feige, Jerome N -- Lagouge, Marie -- Noriega, Lilia -- Milne, Jill C -- Elliott, Peter J -- Puigserver, Pere -- Auwerx, Johan -- 231138/European Research Council/International -- DK069966/DK/NIDDK NIH HHS/ -- DK59820/DK/NIDDK NIH HHS/ -- England -- Nature. 2009 Apr 23;458(7241):1056-60. doi: 10.1038/nature07813.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM/ULP, 67404 Illkirch, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19262508" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*metabolism ; Acetylation ; Aminoimidazole Carboxamide/analogs & derivatives ; Animals ; Cell Line ; *Energy Metabolism/genetics ; Enzyme Activation ; Forkhead Transcription Factors/genetics ; Gene Expression Regulation ; Genes, Mitochondrial/genetics ; Male ; Mice ; Muscle, Skeletal/cytology/enzymology/metabolism ; Mutation ; NAD/*metabolism ; Oxygen Consumption ; Phosphorylation ; Ribonucleotides ; Sirtuin 1 ; Sirtuins/*metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors ; Transcription, Genetic
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    Materials science: Let assemblies bloom (2009)
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    Publication Date: 2009-02-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tonzani, Stefano -- England -- Nature. 2009 Feb 19;457(7232):974. doi: 10.1038/457974a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19225516" target="_blank"〉PubMed〈/a〉
    Keywords: Colloids/*chemistry ; *Magnetics ; Models, Biological ; Nanostructures/chemistry/ultrastructure ; Particle Size ; Water/chemistry
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    Struggle to translate Darwin's view of concurrency (2009)
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    Publication Date: 2009-04-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kutschera, U -- England -- Nature. 2009 Apr 23;458(7241):967. doi: 10.1038/458967c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19396120" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Competitive Behavior ; Cooperative Behavior ; History, 19th Century ; Models, Biological ; *Selection, Genetic ; *Translating ; *Translations
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    The RNA-binding protein KSRP promotes the biogenesis of a subset of microRNAs (2009)
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    Publication Date: 2009-05-22
    Description: Consistent with the role of microRNAs (miRNAs) in down-regulating gene expression by reducing the translation and/or stability of target messenger RNAs, the levels of specific miRNAs are important for correct embryonic development and have been linked to several forms of cancer. However, the regulatory mechanisms by which primary miRNAs (pri-miRNAs) are processed first to precursor miRNAs (pre-miRNAs) and then to mature miRNAs by the multiprotein Drosha and Dicer complexes, respectively, remain largely unknown. The KH-type splicing regulatory protein (KSRP, also known as KHSRP) interacts with single-strand AU-rich-element-containing mRNAs and is a key mediator of mRNA decay. Here we show in mammalian cells that KSRP also serves as a component of both Drosha and Dicer complexes and regulates the biogenesis of a subset of miRNAs. KSRP binds with high affinity to the terminal loop of the target miRNA precursors and promotes their maturation. This mechanism is required for specific changes in target mRNA expression that affect specific biological programs, including proliferation, apoptosis and differentiation. These findings reveal an unexpected mechanism that links KSRP to the machinery regulating maturation of a cohort of miRNAs that, in addition to its role in promoting mRNA decay, independently serves to integrate specific regulatory programs of protein expression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768332/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768332/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trabucchi, Michele -- Briata, Paola -- Garcia-Mayoral, Mariaflor -- Haase, Astrid D -- Filipowicz, Witold -- Ramos, Andres -- Gherzi, Roberto -- Rosenfeld, Michael G -- 082088/Wellcome Trust/United Kingdom -- DK018477/DK/NIDDK NIH HHS/ -- DK39949/DK/NIDDK NIH HHS/ -- GFP04003/Telethon/Italy -- HL065445/HL/NHLBI NIH HHS/ -- MC_U117533887/Medical Research Council/United Kingdom -- MC_U117574558/Medical Research Council/United Kingdom -- R37 DK039949/DK/NIDDK NIH HHS/ -- R37 DK039949-26/DK/NIDDK NIH HHS/ -- R37 DK039949-27/DK/NIDDK NIH HHS/ -- WT022088MA/Wellcome Trust/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jun 18;459(7249):1010-4. doi: 10.1038/nature08025. Epub 2009 May 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department and School of Medicine, University of California, San Diego, 9500 Gilman Drive, Room 345, La Jolla, California 92093-0648, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19458619" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Mice ; MicroRNAs/*biosynthesis/genetics/metabolism ; RNA Processing, Post-Transcriptional ; RNA-Binding Proteins/*metabolism ; Ribonuclease III/chemistry/metabolism ; Trans-Activators/*metabolism
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    Bone-marrow adipocytes as negative regulators of the haematopoietic microenvironment (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-06-12
    Description: Osteoblasts and endothelium constitute functional niches that support haematopoietic stem cells in mammalian bone marrow. Adult bone marrow also contains adipocytes, the number of which correlates inversely with the haematopoietic activity of the marrow. Fatty infiltration of haematopoietic red marrow follows irradiation or chemotherapy and is a diagnostic feature in biopsies from patients with marrow aplasia. To explore whether adipocytes influence haematopoiesis or simply fill marrow space, we compared the haematopoietic activity of distinct regions of the mouse skeleton that differ in adiposity. Here we show, by flow cytometry, colony-forming activity and competitive repopulation assay, that haematopoietic stem cells and short-term progenitors are reduced in frequency in the adipocyte-rich vertebrae of the mouse tail relative to the adipocyte-free vertebrae of the thorax. In lipoatrophic A-ZIP/F1 'fatless' mice, which are genetically incapable of forming adipocytes, and in mice treated with the peroxisome proliferator-activated receptor-gamma inhibitor bisphenol A diglycidyl ether, which inhibits adipogenesis, marrow engraftment after irradiation is accelerated relative to wild-type or untreated mice. These data implicate adipocytes as predominantly negative regulators of the bone-marrow microenvironment, and indicate that antagonizing marrow adipogenesis may enhance haematopoietic recovery in clinical bone-marrow transplantation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831539/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831539/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naveiras, Olaia -- Nardi, Valentina -- Wenzel, Pamela L -- Hauschka, Peter V -- Fahey, Frederic -- Daley, George Q -- DP1 OD000256/OD/NIH HHS/ -- DP1 OD000256-01/OD/NIH HHS/ -- R01 DK059279/DK/NIDDK NIH HHS/ -- R01 DK059279-06/DK/NIDDK NIH HHS/ -- R01 DK070055/DK/NIDDK NIH HHS/ -- R01 DK070055-01/DK/NIDDK NIH HHS/ -- T32- HL -7623/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jul 9;460(7252):259-63. doi: 10.1038/nature08099. Epub 2009 Jun 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pediatric Hematology/Oncology, Children's Hospital Boston and Dana Farber Cancer Institute, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19516257" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/drug effects/*physiology ; Adipogenesis/drug effects ; Adiposity/physiology ; Animals ; Benzhydryl Compounds ; Bone Marrow Cells/*cytology/*metabolism ; Bone Marrow Transplantation ; Cell Line ; Epoxy Compounds/pharmacology ; Femur ; *Hematopoiesis/drug effects ; Hematopoietic Stem Cells/cytology/metabolism ; Homeostasis ; Mice ; Mice, Inbred C57BL ; Osteogenesis ; Spine/cytology/metabolism ; Stromal Cells ; Tail ; Thorax ; Tibia
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    Continuous single-cell imaging of blood generation from haemogenic endothelium (2009)
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    Publication Date: 2009-02-13
    Description: Despite decades of research, the identity of the cells generating the first haematopoietic cells in mammalian embryos is unknown. Indeed, whether blood cells arise from mesodermal cells, mesenchymal progenitors, bipotent endothelial-haematopoietic precursors or haemogenic endothelial cells remains controversial. Proximity of endothelial and blood cells at sites of embryonic haematopoiesis, as well as their similar gene expression, led to the hypothesis of the endothelium generating blood. However, owing to lacking technology it has been impossible to observe blood cell emergence continuously at the single-cell level, and the postulated existence of haemogenic endothelial cells remains disputed. Here, using new imaging and cell-tracking methods, we show that embryonic endothelial cells can be haemogenic. By continuous long-term single-cell observation of mouse mesodermal cells generating endothelial cell and blood colonies, it was possible to detect haemogenic endothelial cells giving rise to blood cells. Living endothelial and haematopoietic cells were identified by simultaneous detection of morphology and multiple molecular and functional markers. Detachment of nascent blood cells from endothelium is not directly linked to asymmetric cell division, and haemogenic endothelial cells are specified from cells already expressing endothelial markers. These results improve our understanding of the developmental origin of mammalian blood and the potential generation of haematopoietic stem cells from embryonic stem cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eilken, Hanna M -- Nishikawa, Shin-Ichi -- Schroeder, Timm -- England -- Nature. 2009 Feb 12;457(7231):896-900. doi: 10.1038/nature07760.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Stem Cell Research, Helmholtz Center Munich-German Research Center for Environmental Health (GmbH), 85764 Neuherberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19212410" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Cells/*cytology ; *Cell Differentiation ; Cell Line ; Embryo, Mammalian/cytology/embryology ; Embryonic Stem Cells/cytology ; Hemangioblasts/*cytology ; *Image Processing, Computer-Assisted ; Mesoderm/cytology ; Mice ; Microscopy, Fluorescence ; *Video Recording
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    Direct cell reprogramming is a stochastic process amenable to acceleration (2009)
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    Publication Date: 2009-11-10
    Description: Direct reprogramming of somatic cells into induced pluripotent stem (iPS) cells can be achieved by overexpression of Oct4, Sox2, Klf4 and c-Myc transcription factors, but only a minority of donor somatic cells can be reprogrammed to pluripotency. Here we demonstrate that reprogramming by these transcription factors is a continuous stochastic process where almost all mouse donor cells eventually give rise to iPS cells on continued growth and transcription factor expression. Additional inhibition of the p53/p21 pathway or overexpression of Lin28 increased the cell division rate and resulted in an accelerated kinetics of iPS cell formation that was directly proportional to the increase in cell proliferation. In contrast, Nanog overexpression accelerated reprogramming in a predominantly cell-division-rate-independent manner. Quantitative analyses define distinct cell-division-rate-dependent and -independent modes for accelerating the stochastic course of reprogramming, and suggest that the number of cell divisions is a key parameter driving epigenetic reprogramming to pluripotency.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789972/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789972/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanna, Jacob -- Saha, Krishanu -- Pando, Bernardo -- van Zon, Jeroen -- Lengner, Christopher J -- Creyghton, Menno P -- van Oudenaarden, Alexander -- Jaenisch, Rudolf -- R01 CA087869/CA/NCI NIH HHS/ -- R01 CA087869-09/CA/NCI NIH HHS/ -- R01 HD045022/HD/NICHD NIH HHS/ -- R01 HD045022-06/HD/NICHD NIH HHS/ -- R01-CA087869/CA/NCI NIH HHS/ -- R01-HDO45022/PHS HHS/ -- R37 CA084198/CA/NCI NIH HHS/ -- R37 CA084198-09/CA/NCI NIH HHS/ -- R37-CA084198/CA/NCI NIH HHS/ -- U54CA143874/CA/NCI NIH HHS/ -- England -- Nature. 2009 Dec 3;462(7273):595-601. doi: 10.1038/nature08592. Epub 2009 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA. Hanna@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19898493" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Division ; Cell Line ; *Cellular Reprogramming ; Gene Expression Regulation, Developmental ; Mice ; Mice, SCID ; Models, Biological ; Pluripotent Stem Cells/*cytology/*metabolism ; Time Factors ; Transcription Factors/genetics/metabolism
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    Biomechanical forces promote embryonic haematopoiesis (2009)
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    Publication Date: 2009-05-15
    Description: Biomechanical forces are emerging as critical regulators of embryogenesis, particularly in the developing cardiovascular system. After initiation of the heartbeat in vertebrates, cells lining the ventral aspect of the dorsal aorta, the placental vessels, and the umbilical and vitelline arteries initiate expression of the transcription factor Runx1 (refs 3-5), a master regulator of haematopoiesis, and give rise to haematopoietic cells. It remains unknown whether the biomechanical forces imposed on the vascular wall at this developmental stage act as a determinant of haematopoietic potential. Here, using mouse embryonic stem cells differentiated in vitro, we show that fluid shear stress increases the expression of Runx1 in CD41(+)c-Kit(+) haematopoietic progenitor cells, concomitantly augmenting their haematopoietic colony-forming potential. Moreover, we find that shear stress increases haematopoietic colony-forming potential and expression of haematopoietic markers in the para-aortic splanchnopleura/aorta-gonads-mesonephros of mouse embryos and that abrogation of nitric oxide, a mediator of shear-stress-induced signalling, compromises haematopoietic potential in vitro and in vivo. Collectively, these data reveal a critical role for biomechanical forces in haematopoietic development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782763/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782763/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adamo, Luigi -- Naveiras, Olaia -- Wenzel, Pamela L -- McKinney-Freeman, Shannon -- Mack, Peter J -- Gracia-Sancho, Jorge -- Suchy-Dicey, Astrid -- Yoshimoto, Momoko -- Lensch, M William -- Yoder, Mervin C -- Garcia-Cardena, Guillermo -- Daley, George Q -- R01 AI080759/AI/NIAID NIH HHS/ -- R01 AI080759-01/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jun 25;459(7250):1131-5. doi: 10.1038/nature08073. Epub 2009 May 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19440194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/cytology/embryology ; *Cell Differentiation ; Cell Line ; Cells, Cultured ; Core Binding Factor Alpha 2 Subunit/genetics ; Embryonic Stem Cells ; Endothelium-Dependent Relaxing Factors/pharmacology ; Female ; Gene Expression Regulation, Developmental ; Hematopoiesis/*physiology ; Hematopoietic Stem Cells/*cytology/drug effects ; Mice ; Nitric Oxide/pharmacology ; Pregnancy ; *Stress, Mechanical
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    Evolutionary diversification in stickleback affects ecosystem functioning (2009)
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    Publication Date: 2009-04-03
    Description: Explaining the ecological causes of evolutionary diversification is a major focus of biology, but surprisingly little has been said about the effects of evolutionary diversification on ecosystems. The number of species in an ecosystem and their traits are key predictors of many ecosystem-level processes, such as rates of productivity, biomass sequestration and decomposition. Here we demonstrate short-term ecosystem-level effects of adaptive radiation in the threespine stickleback (Gasterosteus aculeatus) over the past 10,000 years. These fish have undergone recent parallel diversification in several lakes in coastal British Columbia, resulting in the formation of two specialized species (benthic and limnetic) from a generalist ancestor. Using a mesocosm experiment, we demonstrate that this diversification has strong effects on ecosystems, affecting prey community structure, total primary production, and the nature of dissolved organic materials that regulate the spectral properties of light transmission in the system. However, these ecosystem effects do not simply increase in their relative strength with increasing specialization and species richness; instead, they reflect the complex and indirect consequences of ecosystem engineering by sticklebacks. It is well known that ecological factors influence adaptive radiation. We demonstrate that adaptive radiation, even over short timescales, can have profound effects on ecosystems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harmon, Luke J -- Matthews, Blake -- Des Roches, Simone -- Chase, Jonathan M -- Shurin, Jonathan B -- Schluter, Dolph -- England -- Nature. 2009 Apr 30;458(7242):1167-70. doi: 10.1038/nature07974. Epub 2009 Apr 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Idaho, Moscow, Idaho 83844-3051, USA. lukeh@uidaho.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19339968" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; *Biological Evolution ; Biomass ; British Columbia ; *Ecosystem ; Fishes/*classification/*physiology ; Food Chain ; Fresh Water ; Genetic Speciation ; Models, Biological ; Population Density ; Predatory Behavior
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    The haemangioblast generates haematopoietic cells through a haemogenic endothelium stage (2009)
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    Publication Date: 2009-02-03
    Description: It has been proposed that during embryonic development haematopoietic cells arise from a mesodermal progenitor with both endothelial and haematopoietic potential called the haemangioblast. A conflicting theory instead associates the first haematopoietic cells with a phenotypically differentiated endothelial cell that has haematopoietic potential (that is, a haemogenic endothelium). Support for the haemangioblast concept was initially provided by the identification during mouse embryonic stem cell differentiation of a clonal precursor, the blast colony-forming cell (BL-CFC), which gives rise to blast colonies with both endothelial and haematopoietic components. Although recent studies have now provided evidence for the presence of this bipotential precursor in vivo, the precise mechanism for generation of haematopoietic cells from the haemangioblast still remains completely unknown. Here we demonstrate that the haemangioblast generates haematopoietic cells through the formation of a haemogenic endothelium intermediate, providing the first direct link between these two precursor populations. The cell population containing the haemogenic endothelium is transiently generated during BL-CFC development. This cell population is also present in gastrulating mouse embryos and generates haematopoietic cells on further culture. At the molecular level, we demonstrate that the transcription factor Tal1 (also known as Scl; ref. 10) is indispensable for the establishment of this haemogenic endothelium population whereas the core binding factor Runx1 (also known as AML1; ref. 11) is critical for generation of definitive haematopoietic cells from haemogenic endothelium. Together our results merge the two a priori conflicting theories on the origin of haematopoietic development into a single linear developmental process.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661201/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661201/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lancrin, Christophe -- Sroczynska, Patrycja -- Stephenson, Catherine -- Allen, Terry -- Kouskoff, Valerie -- Lacaud, Georges -- A5297/Cancer Research UK/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2009 Feb 12;457(7231):892-5. doi: 10.1038/nature07679. Epub 2009 Jan 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK Stem Cell Biology Group.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19182774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Core Binding Factor Alpha 2 Subunit/metabolism ; Embryo, Mammalian/cytology/embryology ; Gene Expression Regulation, Developmental ; Hemangioblasts/*cytology ; Hematopoietic Stem Cells/*cytology ; Mice ; Mice, Inbred ICR ; Oncogene Proteins, Fusion/metabolism
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    Antioxidant and oncogene rescue of metabolic defects caused by loss of matrix attachment (2009)
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    Publication Date: 2009-08-21
    Description: Normal epithelial cells require matrix attachment for survival, and the ability of tumour cells to survive outside their natural extracellular matrix (ECM) niches is dependent on acquisition of anchorage independence. Although apoptosis is the most rapid mechanism for eliminating cells lacking appropriate ECM attachment, recent reports suggest that non-apoptotic death processes prevent survival when apoptosis is inhibited in matrix-deprived cells. Here we demonstrate that detachment of mammary epithelial cells from ECM causes an ATP deficiency owing to the loss of glucose transport. Overexpression of ERBB2 rescues the ATP deficiency by restoring glucose uptake through stabilization of EGFR and phosphatidylinositol-3-OH kinase (PI(3)K) activation, and this rescue is dependent on glucose-stimulated flux through the antioxidant-generating pentose phosphate pathway. Notably, we found that the ATP deficiency could be rescued by antioxidant treatment without rescue of glucose uptake. This rescue was found to be dependent on stimulation of fatty acid oxidation, which is inhibited by detachment-induced reactive oxygen species (ROS). The significance of these findings was supported by evidence of an increase in ROS in matrix-deprived cells in the luminal space of mammary acini, and the discovery that antioxidants facilitate the survival of these cells and enhance anchorage-independent colony formation. These results show both the importance of matrix attachment in regulating metabolic activity and an unanticipated mechanism for cell survival in altered matrix environments by antioxidant restoration of ATP generation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931797/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931797/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schafer, Zachary T -- Grassian, Alexandra R -- Song, Loling -- Jiang, Zhenyang -- Gerhart-Hines, Zachary -- Irie, Hanna Y -- Gao, Sizhen -- Puigserver, Pere -- Brugge, Joan S -- K25 CA100290-03/CA/NCI NIH HHS/ -- K25 CA100290-04/CA/NCI NIH HHS/ -- R01 CA105134/CA/NCI NIH HHS/ -- R01 CA105134-09/CA/NCI NIH HHS/ -- England -- Nature. 2009 Sep 3;461(7260):109-13. doi: 10.1038/nature08268. Epub 2009 Aug 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19693011" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Anoikis/physiology ; Antioxidants/*metabolism ; Breast/cytology/metabolism/pathology ; Breast Neoplasms/metabolism/pathology ; Cell Adhesion ; Cell Line ; Cell Survival ; Enzyme Activation ; Epithelial Cells/cytology/*metabolism/pathology ; Extracellular Matrix/*metabolism ; Fatty Acids/metabolism ; Glucose/metabolism ; Humans ; Oncogenes/genetics/*physiology ; Pentose Phosphate Pathway/physiology ; Phosphatidylinositol 3-Kinases/metabolism ; Reactive Oxygen Species/metabolism ; Receptor, Epidermal Growth Factor/metabolism ; Receptor, ErbB-2/genetics/*metabolism
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    Nucleotides released by apoptotic cells act as a find-me signal to promote phagocytic clearance (2009)
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    Publication Date: 2009-09-11
    Description: Phagocytic removal of apoptotic cells occurs efficiently in vivo such that even in tissues with significant apoptosis, very few apoptotic cells are detectable. This is thought to be due to the release of 'find-me' signals by apoptotic cells that recruit motile phagocytes such as monocytes, macrophages and dendritic cells, leading to the prompt clearance of the dying cells. However, the identity and in vivo relevance of such find-me signals are not well understood. Here, through several lines of evidence, we identify extracellular nucleotides as a critical apoptotic cell find-me signal. We demonstrate the caspase-dependent release of ATP and UTP (in equimolar quantities) during the early stages of apoptosis by primary thymocytes and cell lines. Purified nucleotides at these concentrations were sufficient to induce monocyte recruitment comparable to that of apoptotic cell supernatants. Enzymatic removal of ATP and UTP (by apyrase or the expression of ectopic CD39) abrogated the ability of apoptotic cell supernatants to recruit monocytes in vitro and in vivo. We then identified the ATP/UTP receptor P2Y(2) as a critical sensor of nucleotides released by apoptotic cells using RNA interference-mediated depletion studies in monocytes, and macrophages from P2Y(2)-null mice. The relevance of nucleotides in apoptotic cell clearance in vivo was revealed by two approaches. First, in a murine air-pouch model, apoptotic cell supernatants induced a threefold greater recruitment of monocytes and macrophages than supernatants from healthy cells did; this recruitment was abolished by depletion of nucleotides and was significantly decreased in P2Y(2)(-/-) (also known as P2ry2(-/-)) mice. Second, clearance of apoptotic thymocytes was significantly impaired by either depletion of nucleotides or interference with P2Y receptor function (by pharmacological inhibition or in P2Y(2)(-/-) mice). These results identify nucleotides as a critical find-me cue released by apoptotic cells to promote P2Y(2)-dependent recruitment of phagocytes, and provide evidence for a clear relationship between a find-me signal and efficient corpse clearance in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2851546/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2851546/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elliott, Michael R -- Chekeni, Faraaz B -- Trampont, Paul C -- Lazarowski, Eduardo R -- Kadl, Alexandra -- Walk, Scott F -- Park, Daeho -- Woodson, Robin I -- Ostankovich, Marina -- Sharma, Poonam -- Lysiak, Jeffrey J -- Harden, T Kendall -- Leitinger, Norbert -- Ravichandran, Kodi S -- R01 GM064709/GM/NIGMS NIH HHS/ -- R01 GM064709-07/GM/NIGMS NIH HHS/ -- R01 GM069998/GM/NIGMS NIH HHS/ -- R01 GM069998-04/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Sep 10;461(7261):282-6. doi: 10.1038/nature08296.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19741708" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism/pharmacology/secretion ; Animals ; Apoptosis/*physiology ; Cell Line ; Cells, Cultured ; Chemotactic Factors/metabolism/pharmacology/secretion ; Chemotaxis/drug effects ; Culture Media, Conditioned/chemistry/metabolism/pharmacology ; Humans ; Jurkat Cells ; Macrophage Activation/drug effects ; Macrophages/cytology/drug effects/metabolism ; Mice ; Mice, Inbred C57BL ; Monocytes/cytology/drug effects/metabolism ; Phagocytes/*cytology/drug effects/metabolism ; Phagocytosis/drug effects/*physiology ; Purinergic P2 Receptor Antagonists ; Receptors, Purinergic P2/deficiency/genetics/metabolism ; Receptors, Purinergic P2Y2 ; *Signal Transduction/drug effects ; Thymus Gland/*cytology ; Uridine Triphosphate/*metabolism/pharmacology/secretion
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    Cyclic AMP intoxication of macrophages by a Mycobacterium tuberculosis adenylate cyclase (2009)
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    Publication Date: 2009-06-12
    Description: With 8.9 million new cases and 1.7 million deaths per year, tuberculosis is a leading global killer that has not been effectively controlled. The causative agent, Mycobacterium tuberculosis, proliferates within host macrophages where it modifies both its intracellular and local tissue environment, resulting in caseous granulomas with incomplete bacterial sterilization. Although infection by various mycobacterial species produces a cyclic AMP burst within macrophages that influences cell signalling, the underlying mechanism for the cAMP burst remains unclear. Here we show that among the 17 adenylate cyclase genes present in M. tuberculosis, at least one (Rv0386) is required for virulence. Furthermore, we demonstrate that the Rv0386 adenylate cyclase facilitates delivery of bacterial-derived cAMP into the macrophage cytoplasm. Loss of Rv0386 and the intramacrophage cAMP it delivers results in reductions in TNF-alpha production via the protein kinase A and cAMP response-element-binding protein pathway, decreased immunopathology in animal tissues, and diminished bacterial survival. Direct intoxication of host cells by bacterial-derived cAMP may enable M. tuberculosis to modify both its intracellular and tissue environments to facilitate its long-term survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Agarwal, Nisheeth -- Lamichhane, Gyanu -- Gupta, Radhika -- Nolan, Scott -- Bishai, William R -- AI30036/AI/NIAID NIH HHS/ -- AI36973/AI/NIAID NIH HHS/ -- AI37856/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Jul 2;460(7251):98-102. doi: 10.1038/nature08123. Epub 2009 Jun 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Johns Hopkins School of Medicine, CRB2, Room 1.08, 1550 Orleans Street, Baltimore, Maryland 21231-1044, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19516256" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/genetics/*metabolism ; Animals ; Cell Line ; Cyclic AMP/*metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Cytosol/metabolism/microbiology ; Macrophages/immunology/*metabolism/microbiology/*pathology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mycobacterium tuberculosis/*enzymology/genetics/growth & ; development/*pathogenicity ; Phosphoric Diester Hydrolases/genetics/metabolism ; Phosphorylation ; Tuberculosis/immunology/microbiology/*pathology ; Tumor Necrosis Factor-alpha/biosynthesis/secretion ; Virulence/genetics
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    Uptake through glycoprotein 2 of FimH(+) bacteria by M cells initiates mucosal immune response (2009)
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    Publication Date: 2009-11-13
    Description: The mucosal immune system forms the largest part of the entire immune system, containing about three-quarters of all lymphocytes and producing grams of secretory IgA daily to protect the mucosal surface from pathogens. To evoke the mucosal immune response, antigens on the mucosal surface must be transported across the epithelial barrier into organized lymphoid structures such as Peyer's patches. This function, called antigen transcytosis, is mediated by specialized epithelial M cells. The molecular mechanisms promoting this antigen uptake, however, are largely unknown. Here we report that glycoprotein 2 (GP2), specifically expressed on the apical plasma membrane of M cells among enterocytes, serves as a transcytotic receptor for mucosal antigens. Recombinant GP2 protein selectively bound a subset of commensal and pathogenic enterobacteria, including Escherichia coli and Salmonella enterica serovar Typhimurium (S. Typhimurium), by recognizing FimH, a component of type I pili on the bacterial outer membrane. Consistently, these bacteria were colocalized with endogenous GP2 on the apical plasma membrane as well as in cytoplasmic vesicles in M cells. Moreover, deficiency of bacterial FimH or host GP2 led to defects in transcytosis of type-I-piliated bacteria through M cells, resulting in an attenuation of antigen-specific immune responses in Peyer's patches. GP2 is therefore a previously unrecognized transcytotic receptor on M cells for type-I-piliated bacteria and is a prerequisite for the mucosal immune response to these bacteria. Given that M cells are considered a promising target for oral vaccination against various infectious diseases, the GP2-dependent transcytotic pathway could provide a new target for the development of M-cell-targeted mucosal vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hase, Koji -- Kawano, Kazuya -- Nochi, Tomonori -- Pontes, Gemilson Soares -- Fukuda, Shinji -- Ebisawa, Masashi -- Kadokura, Kazunori -- Tobe, Toru -- Fujimura, Yumiko -- Kawano, Sayaka -- Yabashi, Atsuko -- Waguri, Satoshi -- Nakato, Gaku -- Kimura, Shunsuke -- Murakami, Takaya -- Iimura, Mitsutoshi -- Hamura, Kimiyo -- Fukuoka, Shin-Ichi -- Lowe, Anson W -- Itoh, Kikuji -- Kiyono, Hiroshi -- Ohno, Hiroshi -- DK43294/DK/NIDDK NIH HHS/ -- DK56339/DK/NIDDK NIH HHS/ -- England -- Nature. 2009 Nov 12;462(7270):226-30. doi: 10.1038/nature08529.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Epithelial Immunobiology, Research Center for Allergy and Immunology, RIKEN, Kanagawa 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19907495" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Escherichia coli/genetics/immunology/*metabolism ; Animals ; Antigens, Bacterial/genetics/immunology/*metabolism ; Cell Line ; Epithelial Cells/*immunology/metabolism ; Escherichia coli/immunology/metabolism ; Fimbriae Proteins/genetics/immunology/*metabolism ; GPI-Linked Proteins ; Glycoproteins ; HeLa Cells ; Humans ; Immunity, Mucosal/*immunology ; Intestines/cytology ; Membrane Glycoproteins/*metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Peyer's Patches/*cytology/immunology ; Salmonella typhimurium/genetics/immunology/metabolism ; Substrate Specificity
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    Yurt, Coracle, Neurexin IV and the Na(+),K(+)-ATPase form a novel group of epithelial polarity proteins (2009)
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    Publication Date: 2009-06-26
    Description: The integrity of polarized epithelia is critical for development and human health. Many questions remain concerning the full complement and the function of the proteins that regulate cell polarity. Here we report that the Drosophila FERM proteins Yurt (Yrt) and Coracle (Cora) and the membrane proteins Neurexin IV (Nrx-IV) and Na(+),K(+)-ATPase are a new group of functionally cooperating epithelial polarity proteins. This 'Yrt/Cora group' promotes basolateral membrane stability and shows negative regulatory interactions with the apical determinant Crumbs (Crb). Genetic analyses indicate that Nrx-IV and Na(+),K(+)-ATPase act together with Cora in one pathway, whereas Yrt acts in a second redundant pathway. Moreover, we show that the Yrt/Cora group is essential for epithelial polarity during organogenesis but not when epithelial polarity is first established or during terminal differentiation. This property of Yrt/Cora group proteins explains the recovery of polarity in embryos lacking the function of the Lethal giant larvae (Lgl) group of basolateral polarity proteins. We also find that the mammalian Yrt orthologue EPB41L5 (also known as YMO1 and Limulus) is required for lateral membrane formation, indicating a conserved function of Yrt proteins in epithelial polarity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laprise, Patrick -- Lau, Kimberly M -- Harris, Kathryn P -- Silva-Gagliardi, Nancy F -- Paul, Sarah M -- Beronja, Slobodan -- Beitel, Greg J -- McGlade, C Jane -- Tepass, Ulrich -- England -- Nature. 2009 Jun 25;459(7250):1141-5. doi: 10.1038/nature08067.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19553998" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion Molecules, Neuronal/genetics/*metabolism ; Cell Line ; Cell Polarity ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/*embryology/enzymology/genetics/metabolism ; Epithelium/embryology/*physiology ; Gene Knockdown Techniques ; Membrane Proteins/genetics/*metabolism ; Mutation ; Phenotype ; Sodium-Potassium-Exchanging ATPase/genetics/*metabolism
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    Cell biology: Beyond the prion principle (2009)
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    Publication Date: 2009-06-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aguzzi, Adriano -- England -- Nature. 2009 Jun 18;459(7249):924-5. doi: 10.1038/459924a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19536253" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/metabolism ; Animals ; Humans ; Models, Biological ; Peptides/metabolism ; Prion Diseases/*metabolism/pathology/transmission ; Prions/*chemistry/*metabolism ; Protein Denaturation ; tau Proteins/genetics/metabolism
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    Robust discrimination between self and non-self neurites requires thousands of Dscam1 isoforms (2009)
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    Publication Date: 2009-10-02
    Description: Down Syndrome cell adhesion molecule (Dscam) genes encode neuronal cell recognition proteins of the immunoglobulin superfamily. In Drosophila, Dscam1 generates 19,008 different ectodomains by alternative splicing of three exon clusters, each encoding half or a complete variable immunoglobulin domain. Identical isoforms bind to each other, but rarely to isoforms differing at any one of the variable immunoglobulin domains. Binding between isoforms on opposing membranes promotes repulsion. Isoform diversity provides the molecular basis for neurite self-avoidance. Self-avoidance refers to the tendency of branches from the same neuron (self-branches) to selectively avoid one another. To ensure that repulsion is restricted to self-branches, different neurons express different sets of isoforms in a biased stochastic fashion. Genetic studies demonstrated that Dscam1 diversity has a profound role in wiring the fly brain. Here we show how many isoforms are required to provide an identification system that prevents non-self branches from inappropriately recognizing each other. Using homologous recombination, we generated mutant animals encoding 12, 24, 576 and 1,152 potential isoforms. Mutant animals with deletions encoding 4,752 and 14,256 isoforms were also analysed. Branching phenotypes were assessed in three classes of neurons. Branching patterns improved as the potential number of isoforms increased, and this was independent of the identity of the isoforms. Although branching defects in animals with 1,152 potential isoforms remained substantial, animals with 4,752 isoforms were indistinguishable from wild-type controls. Mathematical modelling studies were consistent with the experimental results that thousands of isoforms are necessary to ensure acquisition of unique Dscam1 identities in many neurons. We conclude that thousands of isoforms are essential to provide neurons with a robust discrimination mechanism to distinguish between self and non-self during self-avoidance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836808/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836808/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hattori, Daisuke -- Chen, Yi -- Matthews, Benjamin J -- Salwinski, Lukasz -- Sabatti, Chiara -- Grueber, Wesley B -- Zipursky, S Lawrence -- F31 NS060341/NS/NINDS NIH HHS/ -- R01 DC006485/DC/NIDCD NIH HHS/ -- R01 DC006485-07/DC/NIDCD NIH HHS/ -- R01 HD040279/HD/NICHD NIH HHS/ -- R01 HD040279-05/HD/NICHD NIH HHS/ -- T32 HD007430/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Oct 1;461(7264):644-8. doi: 10.1038/nature08431.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Howard Hughes Medical Institute, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19794492" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Alternative Splicing ; Animals ; Brain/cytology/metabolism ; Cell Adhesion Molecules/*chemistry/genetics/*metabolism ; Drosophila Proteins/*chemistry/genetics/*metabolism ; Drosophila melanogaster/*cytology/genetics/*metabolism ; Female ; Male ; Models, Biological ; Mushroom Bodies/cytology/metabolism ; Neurites/*metabolism ; Protein Isoforms/chemistry/genetics/metabolism ; Sequence Deletion ; Stochastic Processes
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    Evolution: Mouth to mouth (2009)
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    Publication Date: 2009-09-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nicholls, Henry -- England -- Nature. 2009 Sep 10;461(7261):164-6. doi: 10.1038/461164a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19741680" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Developmental Biology ; Fossils ; Hagfishes/*anatomy & histology/*classification/embryology/genetics ; Head/anatomy & histology ; Humans ; Lampreys/*anatomy & histology/*classification/embryology/genetics ; MicroRNAs/genetics/metabolism ; Models, Biological ; Phylogeny ; Sharks/anatomy & histology/classification/embryology
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    Magnetic assembly of colloidal superstructures with multipole symmetry (2009)
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    Publication Date: 2009-02-20
    Description: The assembly of complex structures out of simple colloidal building blocks is of practical interest for building materials with unique optical properties (for example photonic crystals and DNA biosensors) and is of fundamental importance in improving our understanding of self-assembly processes occurring on molecular to macroscopic length scales. Here we demonstrate a self-assembly principle that is capable of organizing a diverse set of colloidal particles into highly reproducible, rotationally symmetric arrangements. The structures are assembled using the magnetostatic interaction between effectively diamagnetic and paramagnetic particles within a magnetized ferrofluid. The resulting multipolar geometries resemble electrostatic charge configurations such as axial quadrupoles ('Saturn rings'), axial octupoles ('flowers'), linear quadrupoles (poles) and mixed multipole arrangements ('two tone'), which represent just a few examples of the type of structure that can be built using this technique.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Erb, Randall M -- Son, Hui S -- Samanta, Bappaditya -- Rotello, Vincent M -- Yellen, Benjamin B -- England -- Nature. 2009 Feb 19;457(7232):999-1002. doi: 10.1038/nature07766.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Duke University, Department of Mechanical Engineering and Materials Science, Center for Biologically Inspired Materials and Material Systems, Box 90300, Hudson Hall, Durham, North Carolina 27708, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19225522" target="_blank"〉PubMed〈/a〉
    Keywords: Colloids/*chemistry ; *Magnetics ; Microscopy, Electron, Scanning ; Microspheres ; Models, Biological ; Nanostructures/chemistry/ultrastructure ; Particle Size ; Water/chemistry
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    Immortalization eliminates a roadblock during cellular reprogramming into iPS cells (2009)
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    Publication Date: 2009-08-12
    Description: The overexpression of defined transcription factors in somatic cells results in their reprogramming into induced pluripotent stem (iPS) cells. The extremely low efficiency and slow kinetics of in vitro reprogramming suggest that further rare events are required to generate iPS cells. The nature and identity of these events, however, remain elusive. We noticed that the reprogramming potential of primary murine fibroblasts into iPS cells decreases after serial passaging and the concomitant onset of senescence. Consistent with the notion that loss of replicative potential provides a barrier for reprogramming, here we show that cells with low endogenous p19(Arf) (encoded by the Ink4a/Arf locus, also known as Cdkn2a locus) protein levels and immortal fibroblasts deficient in components of the Arf-Trp53 pathway yield iPS cell colonies with up to threefold faster kinetics and at a significantly higher efficiency than wild-type cells, endowing almost every somatic cell with the potential to form iPS cells. Notably, the acute genetic ablation of Trp53 (also known as p53) in cellular subpopulations that normally fail to reprogram rescues their ability to produce iPS cells. Our results show that the acquisition of immortality is a crucial and rate-limiting step towards the establishment of a pluripotent state in somatic cells and underscore the similarities between induced pluripotency and tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987892/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987892/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Utikal, Jochen -- Polo, Jose M -- Stadtfeld, Matthias -- Maherali, Nimet -- Kulalert, Warakorn -- Walsh, Ryan M -- Khalil, Adam -- Rheinwald, James G -- Hochedlinger, Konrad -- DP2 OD003266/OD/NIH HHS/ -- England -- Nature. 2009 Aug 27;460(7259):1145-8. doi: 10.1038/nature08285. Epub 2009 Aug 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, Harvard Stem Cell Institute, 185 Cambridge Street, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19668190" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Aging/*physiology ; Cell Differentiation ; Cell Division ; Cell Line ; Cells, Cultured ; Cellular Reprogramming/*physiology ; Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics/metabolism ; Down-Regulation ; Fibroblasts/cytology/metabolism ; Gene Expression ; Humans ; Keratinocytes ; Kinetics ; Mice ; Mice, SCID ; Pluripotent Stem Cells/*cytology/metabolism ; Tumor Suppressor Protein p53/deficiency/genetics/metabolism
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    Temporally precise in vivo control of intracellular signalling (2009)
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    Publication Date: 2009-03-20
    Description: In the study of complex mammalian behaviours, technological limitations have prevented spatiotemporally precise control over intracellular signalling processes. Here we report the development of a versatile family of genetically encoded optical tools ('optoXRs') that leverage common structure-function relationships among G-protein-coupled receptors (GPCRs) to recruit and control, with high spatiotemporal precision, receptor-initiated biochemical signalling pathways. In particular, we have developed and characterized two optoXRs that selectively recruit distinct, targeted signalling pathways in response to light. The two optoXRs exerted opposing effects on spike firing in nucleus accumbens in vivo, and precisely timed optoXR photostimulation in nucleus accumbens by itself sufficed to drive conditioned place preference in freely moving mice. The optoXR approach allows testing of hypotheses regarding the causal impact of biochemical signalling in behaving mammals, in a targetable and temporally precise manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Airan, Raag D -- Thompson, Kimberly R -- Fenno, Lief E -- Bernstein, Hannah -- Deisseroth, Karl -- England -- Nature. 2009 Apr 23;458(7241):1025-9. doi: 10.1038/nature07926. Epub 2009 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19295515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Line ; Cricetinae ; Cyclic AMP Response Element-Binding Protein/metabolism ; *Genetic Engineering ; Humans ; Intracellular Space/*metabolism/radiation effects ; Mice ; Nucleus Accumbens/cytology/physiology/radiation effects ; Receptors, Adrenergic, alpha-1/genetics/metabolism ; Receptors, Adrenergic, beta-2/genetics/metabolism ; Receptors, G-Protein-Coupled/genetics/*metabolism ; Recombinant Fusion Proteins/genetics/*metabolism ; Reward ; Rhodopsin/genetics/metabolism ; *Signal Transduction/radiation effects ; Structure-Activity Relationship ; Time Factors
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    Neuroscience: Glia - more than just brain glue (2009)
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    Publication Date: 2009-02-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, Nicola J -- Barres, Ben A -- England -- Nature. 2009 Feb 5;457(7230):675-7. doi: 10.1038/457675a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19194443" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/physiology ; Biological Evolution ; Brain/*cytology/embryology/pathology/*physiology ; Cell Communication ; Cell Lineage ; Homeostasis ; Humans ; Models, Biological ; Nerve Net/physiology ; Nervous System Diseases/pathology/physiopathology ; Neural Pathways/physiology ; Neuroglia/classification/cytology/pathology/*physiology ; Neurons/cytology/physiology ; Oligodendroglia/pathology/physiology ; Schwann Cells/pathology/physiology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    ErbB2 resembles an autoinhibited invertebrate epidermal growth factor receptor (2009)
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    Publication Date: 2009-09-01
    Description: The orphan receptor tyrosine kinase ErbB2 (also known as HER2 or Neu) transforms cells when overexpressed, and it is an important therapeutic target in human cancer. Structural studies have suggested that the oncogenic (and ligand-independent) signalling properties of ErbB2 result from the absence of a key intramolecular 'tether' in the extracellular region that autoinhibits other human ErbB receptors, including the epidermal growth factor (EGF) receptor. Although ErbB2 is unique among the four human ErbB receptors, here we show that it is the closest structural relative of the single EGF receptor family member in Drosophila melanogaster (dEGFR). Genetic and biochemical data show that dEGFR is tightly regulated by growth factor ligands, yet a crystal structure shows that it, too, lacks the intramolecular tether seen in human EGFR, ErbB3 and ErbB4. Instead, a distinct set of autoinhibitory interdomain interactions hold unliganded dEGFR in an inactive state. All of these interactions are maintained (and even extended) in ErbB2, arguing against the suggestion that ErbB2 lacks autoinhibition. We therefore suggest that normal and pathogenic ErbB2 signalling may be regulated by ligands in the same way as dEGFR. Our findings have important implications for ErbB2 regulation in human cancer, and for developing therapeutic approaches that target novel aspects of this orphan receptor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2762480/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2762480/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alvarado, Diego -- Klein, Daryl E -- Lemmon, Mark A -- R01 CA079992/CA/NCI NIH HHS/ -- R01 CA079992-09/CA/NCI NIH HHS/ -- R01 CA079992-10/CA/NCI NIH HHS/ -- R01 CA125432/CA/NCI NIH HHS/ -- R01 CA125432-01A1/CA/NCI NIH HHS/ -- R01 CA125432-02/CA/NCI NIH HHS/ -- R01 CA125432-03/CA/NCI NIH HHS/ -- England -- Nature. 2009 Sep 10;461(7261):287-91. doi: 10.1038/nature08297. Epub 2009 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, 809C Stellar-Chance Laboratories, 422 Curie Boulevard, Philadelphia, Pennsylvania 19104-6059, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19718021" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Crystallography, X-Ray ; Drosophila Proteins/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Drosophila melanogaster/chemistry/*metabolism ; Enzyme Activation ; Humans ; Ligands ; Models, Molecular ; Protein Structure, Tertiary ; Receptor, Epidermal Growth Factor/*antagonists & ; inhibitors/chemistry/genetics/*metabolism ; Receptor, ErbB-2/antagonists & inhibitors/*chemistry/*metabolism ; Receptors, Invertebrate Peptide/*antagonists & ; inhibitors/chemistry/genetics/*metabolism ; Scattering, Small Angle ; Solubility ; X-Ray Diffraction
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    A parallel circuit of LIF signalling pathways maintains pluripotency of mouse ES cells (2009)
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    Publication Date: 2009-07-03
    Description: The cytokine leukaemia inhibitory factor (LIF) integrates signals into mouse embryonic stem (ES) cells to maintain pluripotency. Although the Jak-Stat3 pathway is essential and sufficient to mediate LIF signals, it is still unclear how these signals are linked to the core circuitry of pluripotency-associated transcription factors, consisting of Oct3/4 (also called Pou5f1), Sox2 and Nanog. Here we show that two LIF signalling pathways are each connected to the core circuitry via different transcription factors. In mouse ES cells, Klf4 is mainly activated by the Jak-Stat3 pathway and preferentially activates Sox2, whereas Tbx3 is preferentially regulated by the phosphatidylinositol-3-OH kinase-Akt and mitogen-activated protein kinase pathways and predominantly stimulates Nanog. In the absence of LIF, artificial expression of Klf4 or Tbx3 is sufficient to maintain pluripotency while maintaining the expression of Oct3/4. Notably, overexpression of Nanog supports LIF-independent self-renewal of mouse ES cells in the absence of Klf4 and Tbx3 activity. Therefore, Klf4 and Tbx3 are involved in mediating LIF signalling to the core circuitry but are not directly associated with the maintenance of pluripotency, because ES cells keep pluripotency without their expression in the particular context.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Niwa, Hitoshi -- Ogawa, Kazuya -- Shimosato, Daisuke -- Adachi, Kenjiro -- England -- Nature. 2009 Jul 2;460(7251):118-22. doi: 10.1038/nature08113.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Pluripotent Cell Studies, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe 6500047, Japan. niwa@cdb.riken.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19571885" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Embryonic Stem Cells/*cytology/*metabolism ; Gene Expression Regulation ; Homeodomain Proteins/genetics/metabolism ; Janus Kinases/metabolism ; Kruppel-Like Transcription Factors/genetics/metabolism ; Leukemia Inhibitory Factor/*metabolism ; MAP Kinase Signaling System ; Mice ; Phosphatidylinositol 3-Kinases/metabolism ; Pluripotent Stem Cells/*cytology/*metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; STAT3 Transcription Factor/metabolism ; *Signal Transduction ; T-Box Domain Proteins/genetics/metabolism
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    Characterization of two classes of small molecule inhibitors of Arp2/3 complex (2009)
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    Publication Date: 2009-08-04
    Description: Polymerization of actin filaments directed by the actin-related protein (Arp)2/3 complex supports many types of cellular movements. However, questions remain regarding the relative contributions of Arp2/3 complex versus other mechanisms of actin filament nucleation to processes such as path finding by neuronal growth cones; this is because of the lack of simple methods to inhibit Arp2/3 complex reversibly in living cells. Here we describe two classes of small molecules that bind to different sites on the Arp2/3 complex and inhibit its ability to nucleate actin filaments. CK-0944636 binds between Arp2 and Arp3, where it appears to block movement of Arp2 and Arp3 into their active conformation. CK-0993548 inserts into the hydrophobic core of Arp3 and alters its conformation. Both classes of compounds inhibit formation of actin filament comet tails by Listeria and podosomes by monocytes. Two inhibitors with different mechanisms of action provide a powerful approach for studying the Arp2/3 complex in living cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780427/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780427/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nolen, B J -- Tomasevic, N -- Russell, A -- Pierce, D W -- Jia, Z -- McCormick, C D -- Hartman, J -- Sakowicz, R -- Pollard, T D -- F32 GM074374-02/GM/NIGMS NIH HHS/ -- GM-066311/GM/NIGMS NIH HHS/ -- GM074374-02/GM/NIGMS NIH HHS/ -- P01 GM066311/GM/NIGMS NIH HHS/ -- P01 GM066311-01A1/GM/NIGMS NIH HHS/ -- P30 EB009998/EB/NIBIB NIH HHS/ -- England -- Nature. 2009 Aug 20;460(7258):1031-4. doi: 10.1038/nature08231. Epub 2009 Aug 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Cellular and Developmental Biology, Yale University, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19648907" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/drug effects/metabolism ; Actin-Related Protein 2/antagonists & inhibitors/chemistry/metabolism ; Actin-Related Protein 2-3 Complex/*antagonists & inhibitors/chemistry/metabolism ; Actin-Related Protein 3/antagonists & inhibitors/chemistry/metabolism ; Actins/chemistry/metabolism ; Animals ; Biopolymers/chemistry/metabolism ; Cattle ; Cell Line ; Crystallography, X-Ray ; Humans ; Hydrophobic and Hydrophilic Interactions ; Indoles/classification/metabolism/pharmacology ; Listeria/physiology ; Models, Molecular ; Monocytes/immunology ; Protein Conformation/drug effects ; Schizosaccharomyces ; Thiazoles/chemistry/classification/metabolism/pharmacology ; Thiophenes/classification/metabolism/pharmacology
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    Histone modifications at human enhancers reflect global cell-type-specific gene expression (2009)
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    Publication Date: 2009-03-20
    Description: The human body is composed of diverse cell types with distinct functions. Although it is known that lineage specification depends on cell-specific gene expression, which in turn is driven by promoters, enhancers, insulators and other cis-regulatory DNA sequences for each gene, the relative roles of these regulatory elements in this process are not clear. We have previously developed a chromatin-immunoprecipitation-based microarray method (ChIP-chip) to locate promoters, enhancers and insulators in the human genome. Here we use the same approach to identify these elements in multiple cell types and investigate their roles in cell-type-specific gene expression. We observed that the chromatin state at promoters and CTCF-binding at insulators is largely invariant across diverse cell types. In contrast, enhancers are marked with highly cell-type-specific histone modification patterns, strongly correlate to cell-type-specific gene expression programs on a global scale, and are functionally active in a cell-type-specific manner. Our results define over 55,000 potential transcriptional enhancers in the human genome, significantly expanding the current catalogue of human enhancers and highlighting the role of these elements in cell-type-specific gene expression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910248/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910248/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heintzman, Nathaniel D -- Hon, Gary C -- Hawkins, R David -- Kheradpour, Pouya -- Stark, Alexander -- Harp, Lindsey F -- Ye, Zhen -- Lee, Leonard K -- Stuart, Rhona K -- Ching, Christina W -- Ching, Keith A -- Antosiewicz-Bourget, Jessica E -- Liu, Hui -- Zhang, Xinmin -- Green, Roland D -- Lobanenkov, Victor V -- Stewart, Ron -- Thomson, James A -- Crawford, Gregory E -- Kellis, Manolis -- Ren, Bing -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG004037-02/HG/NHGRI NIH HHS/ -- U01 HG003151/HG/NHGRI NIH HHS/ -- U01 HG003151-01/HG/NHGRI NIH HHS/ -- U01 HG003151-01S1/HG/NHGRI NIH HHS/ -- U01 HG003151-02/HG/NHGRI NIH HHS/ -- U01 HG003151-03/HG/NHGRI NIH HHS/ -- U01 HG003151-03S1/HG/NHGRI NIH HHS/ -- U01 HG003151-03S2/HG/NHGRI NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2009 May 7;459(7243):108-12. doi: 10.1038/nature07829. Epub 2009 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, UCSD School of Medicine, 9500 Gilman Drive, La Jolla, California 92093-0653, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19295514" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Line ; *Cell Physiological Phenomena ; Chromatin/genetics ; *Gene Expression Regulation ; Genome, Human/genetics ; HeLa Cells ; Histones/*metabolism ; Humans ; K562 Cells ; Promoter Regions, Genetic/genetics ; Transcription Factors/*genetics/metabolism
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    Structural biology: A channel with a twist (2009)
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    Publication Date: 2009-09-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vasquez, Valeria -- Perozo, Eduardo -- England -- Nature. 2009 Sep 3;461(7260):47-9. doi: 10.1038/461047a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19727188" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*chemistry/*metabolism ; Crystallography, X-Ray ; Ion Channel Gating/*physiology ; Ion Channels/*chemistry/*metabolism ; Models, Biological ; Models, Molecular ; Mycobacterium tuberculosis/chemistry ; Pressure ; Protein Structure, Quaternary ; Staphylococcus aureus/*chemistry
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    Phase-locking and environmental fluctuations generate synchrony in a predator-prey community (2009)
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    Publication Date: 2009-07-25
    Description: Spatially synchronized fluctuations in system state are common in physical and biological systems ranging from individual atoms to species as diverse as viruses, insects and mammals. Although the causal factors are well known for many synchronized phenomena, several processes concurrently have an impact on spatial synchrony of species, making their separate effects and interactions difficult to quantify. Here we develop a general stochastic model of predator-prey spatial dynamics to predict the outcome of a laboratory microcosm experiment testing for interactions among all known synchronizing factors: (1) dispersal of individuals between populations; (2) spatially synchronous fluctuations in exogenous environmental factors (the Moran effect); and (3) interactions with other species (for example, predators) that are themselves spatially synchronized. The Moran effect synchronized populations of the ciliate protist Tetrahymena pyriformis; however, dispersal only synchronized prey populations in the presence of the predator Euplotes patella. Both model and data indicate that synchrony depends on cyclic dynamics generated by the predator. Dispersal, but not the Moran effect, 'phase-locks' cycles, which otherwise become 'decoherent' and drift out of phase. In the absence of cycles, phase-locking is not possible and the synchronizing effect of dispersal is negligible. Interspecific interactions determine population synchrony, not by providing an additional source of synchronized fluctuations, but by altering population dynamics and thereby enhancing the action of dispersal. Our results are robust to wide variation in model parameters representative of many natural predator-prey or host-pathogen systems. This explains why cyclic systems provide many of the most dramatic examples of spatial synchrony in nature.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vasseur, David A -- Fox, Jeremy W -- England -- Nature. 2009 Aug 20;460(7258):1007-10. doi: 10.1038/nature08208. Epub 2009 Jul 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, Yale University, New Haven, Connecticut 06520, USA. david.vasseur@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19626006" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Euplotes/*physiology ; *Food Chain ; Models, Biological ; Population Dynamics ; Predatory Behavior/*physiology ; Stochastic Processes ; Tetrahymena pyriformis/*physiology
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    Activation of CaMKII in single dendritic spines during long-term potentiation (2009)
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    Publication Date: 2009-03-20
    Description: Calcium/calmodulin-dependent kinase II (CaMKII) plays a central part in long-term potentiation (LTP), which underlies some forms of learning and memory. Here we monitored the spatiotemporal dynamics of CaMKII activation in individual dendritic spines during LTP using two-photon fluorescence lifetime imaging microscopy, in combination with two-photon glutamate uncaging. Induction of LTP and associated spine enlargement in single spines triggered transient ( approximately 1 min) CaMKII activation restricted to the stimulated spines. CaMKII in spines was specifically activated by NMDA receptors and L-type voltage-sensitive calcium channels, presumably by nanodomain Ca(2+) near the channels, in response to glutamate uncaging and depolarization, respectively. The high degree of compartmentalization and channel specificity of CaMKII signalling allow stimuli-specific spatiotemporal patterns of CaMKII signalling and may be important for synapse-specificity of synaptic plasticity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719773/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719773/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Seok-Jin R -- Escobedo-Lozoya, Yasmin -- Szatmari, Erzsebet M -- Yasuda, Ryohei -- AS1398/Autism Speaks/ -- R01 MH080047/MH/NIMH NIH HHS/ -- R01 MH080047-01/MH/NIMH NIH HHS/ -- R01 MH080047-02/MH/NIMH NIH HHS/ -- R01MH08004/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Mar 19;458(7236):299-304. doi: 10.1038/nature07842.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19295602" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/antagonists & inhibitors/metabolism ; Calcium Channels, L-Type/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics/*metabolism ; Cell Line ; Cells, Cultured ; Chelating Agents/pharmacology ; Dendritic Spines/*enzymology/*physiology ; Enzyme Activation/drug effects ; Fluorescence ; Fluorescence Resonance Energy Transfer ; Glutamic Acid/metabolism ; Hippocampus/cytology ; Humans ; Kinetics ; Long-Term Potentiation/*physiology ; Photons ; Rats ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism ; Synaptic Potentials/physiology ; Time Factors
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    AIM2 activates the inflammasome and cell death in response to cytoplasmic DNA (2009)
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    Publication Date: 2009-01-23
    Description: Host- and pathogen-associated cytoplasmic double-stranded DNA triggers the activation of a NALP3 (also known as cryopyrin and NLRP3)-independent inflammasome, which activates caspase-1 leading to maturation of pro-interleukin-1beta and inflammation. The nature of the cytoplasmic-DNA-sensing inflammasome is currently unknown. Here we show that AIM2 (absent in melanoma 2), an interferon-inducible HIN-200 family member that contains an amino-terminal pyrin domain and a carboxy-terminal oligonucleotide/oligosaccharide-binding domain, senses cytoplasmic DNA by means of its oligonucleotide/oligosaccharide-binding domain and interacts with ASC (apoptosis-associated speck-like protein containing a CARD) through its pyrin domain to activate caspase-1. The interaction of AIM2 with ASC also leads to the formation of the ASC pyroptosome, which induces pyroptotic cell death in cells containing caspase-1. Knockdown of AIM2 by short interfering RNA reduced inflammasome/pyroptosome activation by cytoplasmic DNA in human and mouse macrophages, whereas stable expression of AIM2 in the non-responsive human embryonic kidney 293T cell line conferred responsiveness to cytoplasmic DNA. Our results show that cytoplasmic DNA triggers formation of the AIM2 inflammasome by inducing AIM2 oligomerization. This study identifies AIM2 as an important inflammasome component that senses potentially dangerous cytoplasmic DNA, leading to activation of the ASC pyroptosome and caspase-1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862225/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862225/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandes-Alnemri, Teresa -- Yu, Je-Wook -- Datta, Pinaki -- Wu, Jianghong -- Alnemri, Emad S -- AG14357/AG/NIA NIH HHS/ -- AR055398/AR/NIAMS NIH HHS/ -- R01 AG014357/AG/NIA NIH HHS/ -- R01 AG014357-11/AG/NIA NIH HHS/ -- R01 AR055398/AR/NIAMS NIH HHS/ -- R01 AR055398-11A2/AR/NIAMS NIH HHS/ -- England -- Nature. 2009 Mar 26;458(7237):509-13. doi: 10.1038/nature07710. Epub 2009 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Center for Apoptosis Research, Kimmel Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19158676" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins ; Caspase 1/metabolism ; Cell Death ; Cell Line ; Cytoplasm/*genetics ; Cytoskeletal Proteins/metabolism ; DNA/immunology/*metabolism ; DNA-Binding Proteins ; Enzyme Activation ; Humans ; Inflammation/*metabolism/*pathology ; Mice ; Nuclear Proteins/chemistry/deficiency/genetics/*metabolism ; Protein Binding
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    Post-publication sharing of data and tools (2009)
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    Publication Date: 2009-09-11
    Description: Despite existing guidelines on access to data and bioresources, good practice is not widespread. A meeting of mouse researchers in Rome proposes ways to promote a culture of sharing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schofield, Paul N -- Bubela, Tania -- Weaver, Thomas -- Portilla, Lili -- Brown, Stephen D -- Hancock, John M -- Einhorn, David -- Tocchini-Valentini, Glauco -- Hrabe de Angelis, Martin -- Rosenthal, Nadia -- CASIMIR Rome Meeting participants -- 062023/Wellcome Trust/United Kingdom -- 077198/Wellcome Trust/United Kingdom -- MC_U142684171/Medical Research Council/United Kingdom -- England -- Nature. 2009 Sep 10;461(7261):171-3. doi: 10.1038/461171a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, CB2 3EG, UK. PS@mole.bio.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19741686" target="_blank"〉PubMed〈/a〉
    Keywords: *Access to Information ; Animals ; Cell Line ; *Cooperative Behavior ; Guidelines as Topic ; Information Storage and Retrieval ; Licensure ; Mice ; Models, Animal ; *Publishing/standards ; *Research/standards ; Research Design ; Rome ; Technology Transfer
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    Bush's legacy: 43 by the numbers (2009)
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    Details
    Publication Date: 2009-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schrope, Mark -- England -- Nature. 2009 Jan 15;457(7227):252-3. doi: 10.1038/457252a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19148075" target="_blank"〉PubMed〈/a〉
    Keywords: Bioterrorism/prevention & control/trends ; Cell Line ; Conservation of Natural Resources/history/trends ; Embryonic Stem Cells/cytology ; Federal Government/*history ; History, 21st Century ; Humans ; Science/economics/*history/trends ; Space Flight/history/trends ; United States
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Reconstitution of Rab- and SNARE-dependent membrane fusion by synthetic endosomes (2009)
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    Publication Date: 2009-05-22
    Description: Rab GTPases and SNAREs (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) are evolutionarily conserved essential components of the eukaryotic intracellular transport system. Although pairing of cognate SNAREs is sufficient to fuse membranes in vitro, a complete reconstitution of the Rab-SNARE machinery has never been achieved. Here we report the reconstitution of the early endosomal canine Rab5 GTPase, its key regulators and effectors together with SNAREs into proteoliposomes using a set of 17 recombinant human proteins. These vesicles behave like minimal 'synthetic' endosomes, fusing with purified early endosomes or with each other in vitro. Membrane fusion measured by content-mixing and morphological assays requires the cooperativity between Rab5 effectors and cognate SNAREs which, together, form a more efficient 'core machinery' than SNAREs alone. In reconstituting a fusion mechanism dependent on both a Rab GTPase and SNAREs, our work shows that the two machineries act coordinately to increase the specificity and efficiency of the membrane tethering and fusion process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohya, Takeshi -- Miaczynska, Marta -- Coskun, Unal -- Lommer, Barbara -- Runge, Anja -- Drechsel, David -- Kalaidzidis, Yannis -- Zerial, Marino -- England -- Nature. 2009 Jun 25;459(7250):1091-7. doi: 10.1038/nature08107. Epub 2009 May 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstrasse 108, 01309, Dresden, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19458617" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cricetinae ; Cytosol/metabolism ; Dogs ; Endosomes/metabolism/*physiology ; Humans ; Membrane Fusion/*physiology ; Microscopy, Electron ; Proteolipids/metabolism/ultrastructure ; Recombinant Proteins/metabolism ; SNARE Proteins/*metabolism ; Vesicular Transport Proteins/metabolism ; rab GTP-Binding Proteins/*metabolism
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    Regulation of the innate immune response by threonine-phosphatase of Eyes absent (2009)
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    Publication Date: 2009-06-30
    Description: Innate immunity is stimulated not only by viral or bacterial components, but also by non-microbial danger signals (damage-associated molecular patterns). One of the damage-associated molecular patterns is chromosomal DNA that escapes degradation. In programmed cell death and erythropoiesis, DNA from dead cells or nuclei expelled from erythroblasts is digested by DNase II in the macrophages after they are engulfed. DNase II(-/-) (also known as Dnase2a(-/-)) mice suffer from severe anaemia or chronic arthritis due to interferon-beta (IFN-beta) and tumour necrosis factor-alpha (TNF-alpha) produced from the macrophages carrying undigested DNA in a Toll-like receptor (TLR)-independent mechanism. Here we show that Eyes absent 4 (EYA4), originally identified as a co-transcription factor, stimulates the expression of IFN-beta and CXCL10 in response to the undigested DNA of apoptotic cells. EYA4 enhanced the innate immune response against viruses (Newcastle disease virus and vesicular stomatitis virus), and could associate with signalling molecules (IPS-1 (also known as MAVS), STING (TMEM173) and NLRX1). Three groups have previously shown that EYA has phosphatase activity. We found that mouse EYA family members act as a phosphatase for both phosphotyrosine and phosphothreonine. The haloacid dehalogenase domain at the carboxy terminus contained the tyrosine-phosphatase, and the amino-terminal half carried the threonine-phosphatase. Mutations of the threonine-phosphatase, but not the tyrosine-phosphatase, abolished the ability of EYA4 to enhance the innate immune response, suggesting that EYA regulates the innate immune response by modulating the phosphorylation state of signal transducers for the intracellular pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okabe, Yasutaka -- Sano, Teruyuki -- Nagata, Shigekazu -- England -- Nature. 2009 Jul 23;460(7254):520-4. doi: 10.1038/nature08138. Epub 2009 Jun 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19561593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Line ; Chemokine CXCL10/metabolism ; Gene Expression Regulation/*immunology ; Humans ; Immunity, Innate/*immunology ; Interferon-beta/metabolism ; Membrane Proteins/metabolism ; Mice ; Mitochondrial Proteins/metabolism ; Phosphoprotein Phosphatases/*metabolism ; Signal Transduction ; Trans-Activators/*metabolism
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    An unusual carbon-carbon bond cleavage reaction during phosphinothricin biosynthesis (2009)
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    Publication Date: 2009-06-12
    Description: Natural products containing phosphorus-carbon bonds have found widespread use in medicine and agriculture. One such compound, phosphinothricin tripeptide, contains the unusual amino acid phosphinothricin attached to two alanine residues. Synthetic phosphinothricin (glufosinate) is a component of two top-selling herbicides (Basta and Liberty), and is widely used with resistant transgenic crops including corn, cotton and canola. Recent genetic and biochemical studies showed that during phosphinothricin tripeptide biosynthesis 2-hydroxyethylphosphonate (HEP) is converted to hydroxymethylphosphonate (HMP). Here we report the in vitro reconstitution of this unprecedented C(sp(3))-C(sp(3)) bond cleavage reaction and X-ray crystal structures of the enzyme. The protein is a mononuclear non-haem iron(ii)-dependent dioxygenase that converts HEP to HMP and formate. In contrast to most other members of this family, the oxidative consumption of HEP does not require additional cofactors or the input of exogenous electrons. The current study expands the scope of reactions catalysed by the 2-His-1-carboxylate mononuclear non-haem iron family of enzymes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874955/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874955/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cicchillo, Robert M -- Zhang, Houjin -- Blodgett, Joshua A V -- Whitteck, John T -- Li, Gongyong -- Nair, Satish K -- van der Donk, Wilfred A -- Metcalf, William W -- P01 GM077596/GM/NIGMS NIH HHS/ -- P01 GM077596-03/GM/NIGMS NIH HHS/ -- R01 GM059334/GM/NIGMS NIH HHS/ -- R01 GM059334-09/GM/NIGMS NIH HHS/ -- R01 GM59334/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Jun 11;459(7248):871-4. doi: 10.1038/nature07972.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19516340" target="_blank"〉PubMed〈/a〉
    Keywords: Aminobutyrates/*chemistry/*metabolism ; Biocatalysis ; Crystallography, X-Ray ; Dioxygenases/chemistry/genetics/*metabolism ; Escherichia coli ; Formates/metabolism ; Magnetic Resonance Spectroscopy ; Mass Spectrometry ; Models, Biological ; Models, Molecular ; Molecular Conformation ; Organophosphonates/metabolism
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    The importance of niches for the maintenance of species diversity (2009)
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    Publication Date: 2009-08-14
    Description: Ecological communities characteristically contain a wide diversity of species with important functional, economic and aesthetic value. Ecologists have long questioned how this diversity is maintained. Classic theory shows that stable coexistence requires competitors to differ in their niches; this has motivated numerous investigations of ecological differences presumed to maintain diversity. That niche differences are key to coexistence, however, has recently been challenged by the neutral theory of biodiversity, which explains coexistence with the equivalence of competitors. The ensuing controversy has motivated calls for a better understanding of the collective importance of niche differences for the diversity observed in ecological communities. Here we integrate theory and experimentation to show that niche differences collectively stabilize the dynamics of experimental communities of serpentine annual plants. We used field-parameterized population models to develop a null expectation for community dynamics without the stabilizing effects of niche differences. The population growth rates predicted by this null model varied by several orders of magnitude between species, which is sufficient for rapid competitive exclusion. Moreover, after two generations of community change in the field, Shannon diversity was over 50 per cent greater in communities stabilized by niche differences relative to those exhibiting dynamics predicted by the null model. Finally, in an experiment manipulating species' relative abundances, population growth rates increased when species became rare--the demographic signature of niche differences. Our work thus provides strong evidence that species differences have a critical role in stabilizing species diversity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, Jonathan M -- HilleRisLambers, Janneke -- England -- Nature. 2009 Sep 10;461(7261):254-7. doi: 10.1038/nature08251. Epub 2009 Aug 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology, Evolution, and Marine Biology, University of California, Santa Barbara, California 93106, USA. levine@lifesci.ucsb.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19675568" target="_blank"〉PubMed〈/a〉
    Keywords: *Biodiversity ; California ; *Ecosystem ; Models, Biological ; Plant Development ; *Plant Physiological Phenomena ; Plants/classification ; Population Dynamics ; Seeds/physiology
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    Increasing carbon storage in intact African tropical forests (2009)
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    Publication Date: 2009-02-20
    Description: The response of terrestrial vegetation to a globally changing environment is central to predictions of future levels of atmospheric carbon dioxide. The role of tropical forests is critical because they are carbon-dense and highly productive. Inventory plots across Amazonia show that old-growth forests have increased in carbon storage over recent decades, but the response of one-third of the world's tropical forests in Africa is largely unknown owing to an absence of spatially extensive observation networks. Here we report data from a ten-country network of long-term monitoring plots in African tropical forests. We find that across 79 plots (163 ha) above-ground carbon storage in live trees increased by 0.63 Mg C ha(-1) yr(-1) between 1968 and 2007 (95% confidence interval (CI), 0.22-0.94; mean interval, 1987-96). Extrapolation to unmeasured forest components (live roots, small trees, necromass) and scaling to the continent implies a total increase in carbon storage in African tropical forest trees of 0.34 Pg C yr(-1) (CI, 0.15-0.43). These reported changes in carbon storage are similar to those reported for Amazonian forests per unit area, providing evidence that increasing carbon storage in old-growth forests is a pan-tropical phenomenon. Indeed, combining all standardized inventory data from this study and from tropical America and Asia together yields a comparable figure of 0.49 Mg C ha(-1) yr(-1) (n = 156; 562 ha; CI, 0.29-0.66; mean interval, 1987-97). This indicates a carbon sink of 1.3 Pg C yr(-1) (CI, 0.8-1.6) across all tropical forests during recent decades. Taxon-specific analyses of African inventory and other data suggest that widespread changes in resource availability, such as increasing atmospheric carbon dioxide concentrations, may be the cause of the increase in carbon stocks, as some theory and models predict.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewis, Simon L -- Lopez-Gonzalez, Gabriela -- Sonke, Bonaventure -- Affum-Baffoe, Kofi -- Baker, Timothy R -- Ojo, Lucas O -- Phillips, Oliver L -- Reitsma, Jan M -- White, Lee -- Comiskey, James A -- Djuikouo K, Marie-Noel -- Ewango, Corneille E N -- Feldpausch, Ted R -- Hamilton, Alan C -- Gloor, Manuel -- Hart, Terese -- Hladik, Annette -- Lloyd, Jon -- Lovett, Jon C -- Makana, Jean-Remy -- Malhi, Yadvinder -- Mbago, Frank M -- Ndangalasi, Henry J -- Peacock, Julie -- Peh, Kelvin S-H -- Sheil, Douglas -- Sunderland, Terry -- Swaine, Michael D -- Taplin, James -- Taylor, David -- Thomas, Sean C -- Votere, Raymond -- Woll, Hannsjorg -- England -- Nature. 2009 Feb 19;457(7232):1003-6. doi: 10.1038/nature07771.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Earth and Biosphere Institute, School of Geography, University of Leeds, Leeds LS2 9JT, UK. s.l.lewis@leeds.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19225523" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Atmosphere/chemistry ; Biomass ; Carbon/analysis/*metabolism ; Carbon Dioxide/analysis/metabolism ; Models, Biological ; Trees/anatomy & histology/chemistry/growth & development/*metabolism ; *Tropical Climate ; Wilderness ; Wood/analysis/chemistry
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    Biomechanics: Serpentine steps (2009)
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    Publication Date: 2009-06-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, Andrew J -- Summers, Adam P -- England -- Nature. 2009 Jun 18;459(7249):919-20. doi: 10.1038/459919a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19536249" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomechanical Phenomena ; Body Weight ; Friction ; Gait/physiology ; Locomotion/*physiology ; Models, Biological ; Snakes/*physiology
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    Germline-encoded amino acids in the alphabeta T-cell receptor control thymic selection (2009)
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    Publication Date: 2009-03-06
    Description: An alphabeta T-cell response depends on the recognition of antigen plus major histocompatibility complex (MHC) proteins by its antigen receptor (TCR). The ability of peripheral alphabeta T cells to recognize MHC is at least partly determined by MHC-dependent thymic selection, by which an immature T cell survives only if its TCR can recognize self MHC. This process may allow MHC-reactive TCRs to be selected from a repertoire with completely random and unbiased specificities. However, analysis of thymocytes before positive selection indicated that TCR proteins might have a predetermined ability to bind MHC. Here we show that specific germline-encoded amino acids in the TCR promote 'generic' MHC recognition and control thymic selection. In mice expressing single, rearranged TCR beta-chains, individual mutation of amino acids in the complementarity-determining region (CDR) 2beta to Ala reduced development of the entire TCR repertoire. Altogether, these results show that thymic selection is controlled by germline-encoded MHC contact points in the alphabeta TCR and indicate that the diversity of the peripheral T-cell repertoire is enhanced by this 'built-in' specificity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2679808/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2679808/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott-Browne, James P -- White, Janice -- Kappler, John W -- Gapin, Laurent -- Marrack, Philippa -- AI057485/AI/NIAID NIH HHS/ -- AI18785/AI/NIAID NIH HHS/ -- AI22295/AI/NIAID NIH HHS/ -- P01 AI022295/AI/NIAID NIH HHS/ -- P01 AI022295-22/AI/NIAID NIH HHS/ -- P30 CA046934/CA/NCI NIH HHS/ -- P30 CA046934-19/CA/NCI NIH HHS/ -- P30 CA046934-20/CA/NCI NIH HHS/ -- P30 CA046934-21/CA/NCI NIH HHS/ -- R01 AI018785/AI/NIAID NIH HHS/ -- R01 AI018785-26/AI/NIAID NIH HHS/ -- R01 AI057485/AI/NIAID NIH HHS/ -- R01 AI057485-05/AI/NIAID NIH HHS/ -- R21 AI076463/AI/NIAID NIH HHS/ -- R21 AI076463-01A1/AI/NIAID NIH HHS/ -- R56 AI017134/AI/NIAID NIH HHS/ -- R56 AI017134-28/AI/NIAID NIH HHS/ -- T32 AI007405/AI/NIAID NIH HHS/ -- T32 AI007405-17/AI/NIAID NIH HHS/ -- T32 AI007405-18/AI/NIAID NIH HHS/ -- T32 AI07405/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Apr 23;458(7241):1043-6. doi: 10.1038/nature07812. Epub 2009 Mar 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Integrated Department of Immunology, National Jewish Health and University of Colorado Denver, Denver, Colorado 80206, USA. james.scott-browne@ucdenver.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19262510" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/*genetics/*metabolism ; Animals ; Bone Marrow/immunology/metabolism ; Cell Line ; Chimera/immunology/metabolism ; Complementarity Determining Regions/chemistry/genetics/immunology ; Germ Cells/*metabolism ; Hybridomas/immunology ; Major Histocompatibility Complex/immunology ; Mice ; Receptors, Antigen, T-Cell, alpha-beta/*chemistry/deficiency/genetics/*immunology ; Thymus Gland/*cytology/*immunology
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    Ecology: Traits of plant invaders (2009)
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    Publication Date: 2009-06-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seastedt, Tim -- England -- Nature. 2009 Jun 11;459(7248):783-4. doi: 10.1038/459783a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19516327" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Ecosystem ; Europe ; Models, Biological ; *Plant Development ; Plants/*microbiology ; Population Growth ; United States
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    Ecology: Speciation affects ecosystems (2009)
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    Publication Date: 2009-05-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seehausen, Ole -- England -- Nature. 2009 Apr 30;458(7242):1122-3. doi: 10.1038/4581122a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407790" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; *Biological Evolution ; British Columbia ; *Ecosystem ; Fishes/*classification/*physiology ; Food Chain ; Fresh Water ; Genetic Speciation ; Models, Biological
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    Stem cells: Tailor-made diseased neurons (2009)
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    Publication Date: 2009-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sendtner, Michael -- England -- Nature. 2009 Jan 15;457(7227):269-70. doi: 10.1038/457269a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19148087" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation/drug effects ; Cell Separation ; *Cellular Reprogramming/drug effects ; Child ; Female ; Fibroblasts/cytology ; Humans ; Mice ; Models, Biological ; Motor Neurons/drug effects/metabolism/*pathology ; Muscular Atrophy, Spinal/drug therapy/metabolism/*pathology ; Pluripotent Stem Cells/cytology/drug effects/metabolism/*pathology ; Skin/*cytology ; Survival of Motor Neuron 1 Protein/genetics/metabolism
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    The role of terrestrial plants in limiting atmospheric CO(2) decline over the past 24 million years (2009)
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    Publication Date: 2009-07-03
    Description: Environmental conditions during the past 24 million years are thought to have been favourable for enhanced rates of atmospheric carbon dioxide drawdown by silicate chemical weathering. Proxy records indicate, however, that the Earth's atmospheric carbon dioxide concentrations did not fall below about 200-250 parts per million during this period. The stabilization of atmospheric carbon dioxide concentrations near this minimum value suggests that strong negative feedback mechanisms inhibited further drawdown of atmospheric carbon dioxide by high rates of global silicate rock weathering. Here we investigate one possible negative feedback mechanism, occurring under relatively low carbon dioxide concentrations and in warm climates, that is related to terrestrial plant productivity and its role in the decomposition of silicate minerals. We use simulations of terrestrial and geochemical carbon cycles and available experimental evidence to show that vegetation activity in upland regions of active orogens was severely limited by near-starvation of carbon dioxide in combination with global warmth over this period. These conditions diminished biotic-driven silicate rock weathering and thereby attenuated an important long-term carbon dioxide sink. Although our modelling results are semi-quantitative and do not capture the full range of biogeochemical feedbacks that could influence the climate, our analysis indicates that the dynamic equilibrium between plants, climate and the geosphere probably buffered the minimum atmospheric carbon dioxide concentrations over the past 24 million years.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pagani, Mark -- Caldeira, Ken -- Berner, Robert -- Beerling, David J -- England -- Nature. 2009 Jul 2;460(7251):85-8. doi: 10.1038/nature08133.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geology and Geophysics, Yale University, New Haven, Connecticut 06520, USA. mark.pagani@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19571882" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atmosphere/*chemistry ; Biomass ; Carbon Dioxide/*analysis ; Climate ; Eukaryota ; Geologic Sediments/*chemistry ; Geology ; History, Ancient ; Ice Cover ; Models, Biological ; Plant Leaves/metabolism ; Plant Roots/growth & development ; Plant Transpiration ; Plants/*metabolism ; Silicates/*chemistry
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    US stem-cell research expands (2009)
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    Publication Date: 2009-07-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wadman, Meredith -- England -- Nature. 2009 Jul 9;460(7252):156-7. doi: 10.1038/460156a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19587729" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Embryo Research ; *Guidelines as Topic ; Humans ; *National Institutes of Health (U.S.) ; Registries ; *Stem Cells/cytology ; United States
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    Human DNA methylomes at base resolution show widespread epigenomic differences (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-10-16
    Description: DNA cytosine methylation is a central epigenetic modification that has essential roles in cellular processes including genome regulation, development and disease. Here we present the first genome-wide, single-base-resolution maps of methylated cytosines in a mammalian genome, from both human embryonic stem cells and fetal fibroblasts, along with comparative analysis of messenger RNA and small RNA components of the transcriptome, several histone modifications, and sites of DNA-protein interaction for several key regulatory factors. Widespread differences were identified in the composition and patterning of cytosine methylation between the two genomes. Nearly one-quarter of all methylation identified in embryonic stem cells was in a non-CG context, suggesting that embryonic stem cells may use different methylation mechanisms to affect gene regulation. Methylation in non-CG contexts showed enrichment in gene bodies and depletion in protein binding sites and enhancers. Non-CG methylation disappeared upon induced differentiation of the embryonic stem cells, and was restored in induced pluripotent stem cells. We identified hundreds of differentially methylated regions proximal to genes involved in pluripotency and differentiation, and widespread reduced methylation levels in fibroblasts associated with lower transcriptional activity. These reference epigenomes provide a foundation for future studies exploring this key epigenetic modification in human disease and development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2857523/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2857523/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lister, Ryan -- Pelizzola, Mattia -- Dowen, Robert H -- Hawkins, R David -- Hon, Gary -- Tonti-Filippini, Julian -- Nery, Joseph R -- Lee, Leonard -- Ye, Zhen -- Ngo, Que-Minh -- Edsall, Lee -- Antosiewicz-Bourget, Jessica -- Stewart, Ron -- Ruotti, Victor -- Millar, A Harvey -- Thomson, James A -- Ren, Bing -- Ecker, Joseph R -- R01 HG003523/HG/NHGRI NIH HHS/ -- R01 HG003523-01/HG/NHGRI NIH HHS/ -- R01 HG003523-02/HG/NHGRI NIH HHS/ -- R01 HG003523-03/HG/NHGRI NIH HHS/ -- U01 1U01ES017166-01/ES/NIEHS NIH HHS/ -- U01 ES017166/ES/NIEHS NIH HHS/ -- England -- Nature. 2009 Nov 19;462(7271):315-22. doi: 10.1038/nature08514. Epub 2009 Oct 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomic Analysis Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19829295" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cluster Analysis ; DNA/metabolism ; *DNA Methylation ; DNA-Binding Proteins/metabolism ; Embryonic Stem Cells/metabolism ; *Epigenesis, Genetic ; Genome/*genetics ; Humans
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    Something wiki this way comes. Interview by Bryn Nelson (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-03-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friend, Stephen -- Schadt, Eric -- England -- Nature. 2009 Mar 5;458(7234):13. doi: 10.1038/458013a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19262635" target="_blank"〉PubMed〈/a〉
    Keywords: *Access to Information ; Animals ; *Biomedical Research ; Humans ; *Internet ; Mice ; Models, Biological ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Still strict on stem cells (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-04-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wadman, Meredith -- England -- Nature. 2009 Apr 23;458(7241):950-1. doi: 10.1038/458950a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19396105" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryo Research/economics/*legislation & jurisprudence ; *Embryonic Stem Cells ; *Federal Government ; Female ; *Guidelines as Topic/standards ; Humans ; Male ; National Institutes of Health (U.S.)/*legislation & jurisprudence ; United States
    Print ISSN: 0028-0836
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    Discovery of insect and human dengue virus host factors (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-04-28
    Description: Dengue fever is the most frequent arthropod-borne viral disease of humans, with almost half of the world's population at risk of infection. The high prevalence, lack of an effective vaccine, and absence of specific treatment conspire to make dengue fever a global public health threat. Given their compact genomes, dengue viruses (DENV-1-4) and other flaviviruses probably require an extensive number of host factors; however, only a limited number of human, and an even smaller number of insect host factors, have been identified. Here we identify insect host factors required for DENV-2 propagation, by carrying out a genome-wide RNA interference screen in Drosophila melanogaster cells using a well-established 22,632 double-stranded RNA library. This screen identified 116 candidate dengue virus host factors (DVHFs). Although some were previously associated with flaviviruses (for example, V-ATPases and alpha-glucosidases), most of the DVHFs were newly implicated in dengue virus propagation. The dipteran DVHFs had 82 readily recognizable human homologues and, using a targeted short-interfering-RNA screen, we showed that 42 of these are human DVHFs. This indicates notable conservation of required factors between dipteran and human hosts. This work suggests new approaches to control infection in the insect vector and the mammalian host.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462662/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462662/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sessions, October M -- Barrows, Nicholas J -- Souza-Neto, Jayme A -- Robinson, Timothy J -- Hershey, Christine L -- Rodgers, Mary A -- Ramirez, Jose L -- Dimopoulos, George -- Yang, Priscilla L -- Pearson, James L -- Garcia-Blanco, Mariano A -- 1R01AI061576-01/AI/NIAID NIH HHS/ -- 1R01AI076442/AI/NIAID NIH HHS/ -- 1SA0RR024572-1/RR/NCRR NIH HHS/ -- 5P30-CA14236/CA/NCI NIH HHS/ -- 5U54-AI057157-05S/AI/NIAID NIH HHS/ -- R01 AI076442/AI/NIAID NIH HHS/ -- R01 AI078997/AI/NIAID NIH HHS/ -- R01 AI078997-01A1/AI/NIAID NIH HHS/ -- R01 AI078997-02/AI/NIAID NIH HHS/ -- R01 GM067761/GM/NIGMS NIH HHS/ -- R21 AI090188/AI/NIAID NIH HHS/ -- R21 AI090188-01/AI/NIAID NIH HHS/ -- R21 NS063845/NS/NINDS NIH HHS/ -- R21-AI64925/AI/NIAID NIH HHS/ -- T32 AI007417/AI/NIAID NIH HHS/ -- U54 AI057157/AI/NIAID NIH HHS/ -- U54 AI057159/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Apr 23;458(7241):1047-50. doi: 10.1038/nature07967.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19396146" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/genetics/virology ; Animals ; Cell Line ; Conserved Sequence/*genetics/physiology ; Dengue Virus/*physiology ; Drosophila melanogaster/*genetics/physiology/*virology ; Gene Knockdown Techniques ; Genome, Insect/genetics ; Host-Pathogen Interactions/*genetics ; Humans ; Insect Vectors/*genetics/*physiology ; RNA Interference ; RNA, Double-Stranded/genetics/metabolism ; Virus Replication
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    AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-01-23
    Description: The innate immune system senses nucleic acids by germline-encoded pattern recognition receptors. RNA is sensed by Toll-like receptor members TLR3, TLR7 and TLR8, or by the RNA helicases RIG-I (also known as DDX58) and MDA-5 (IFIH1). Little is known about sensors for cytoplasmic DNA that trigger antiviral and/or inflammatory responses. The best characterized of these responses involves activation of the TANK-binding kinase (TBK1)-interferon regulatory factor 3 (IRF3) signalling axis to trigger transcriptional induction of type I interferon genes. A second, less well-defined pathway leads to the activation of an 'inflammasome' that, via caspase-1, controls the catalytic cleavage of the pro-forms of the cytokines IL1beta and IL18 (refs 6, 7). Using mouse and human cells, here we identify the PYHIN (pyrin and HIN domain-containing protein) family member absent in melanoma 2 (AIM2) as a receptor for cytosolic DNA, which regulates caspase-1. The HIN200 domain of AIM2 binds to DNA, whereas the pyrin domain (but not that of the other PYHIN family members) associates with the adaptor molecule ASC (apoptosis-associated speck-like protein containing a caspase activation and recruitment domain) to activate both NF-kappaB and caspase-1. Knockdown of Aim2 abrogates caspase-1 activation in response to cytoplasmic double-stranded DNA and the double-stranded DNA vaccinia virus. Collectively, these observations identify AIM2 as a new receptor for cytoplasmic DNA, which forms an inflammasome with the ligand and ASC to activate caspase-1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726264/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726264/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hornung, Veit -- Ablasser, Andrea -- Charrel-Dennis, Marie -- Bauernfeind, Franz -- Horvath, Gabor -- Caffrey, Daniel R -- Latz, Eicke -- Fitzgerald, Katherine A -- AI-065483/AI/NIAID NIH HHS/ -- AI-067497/AI/NIAID NIH HHS/ -- R01 AI067497/AI/NIAID NIH HHS/ -- R01 AI067497-03/AI/NIAID NIH HHS/ -- R01 AI067497-04/AI/NIAID NIH HHS/ -- R01 AI067497-05/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Mar 26;458(7237):514-8. doi: 10.1038/nature07725. Epub 2009 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA. veit.hornung@uni-bonn.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19158675" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins ; Caspase 1/*metabolism ; Cell Death ; Cell Line ; Cytoskeletal Proteins/genetics/*metabolism ; Cytosol/*metabolism ; DNA/immunology/*metabolism ; DNA-Binding Proteins ; Enzyme Activation ; Humans ; Inflammation/enzymology/*metabolism/pathology ; Mice ; Nuclear Proteins/chemistry/genetics/*metabolism ; Poly dA-dT/immunology ; Protein Binding ; Vaccinia virus/immunology
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    Coordinating DNA replication by means of priming loop and differential synthesis rate (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-11-20
    Description: Genomic DNA is replicated by two DNA polymerase molecules, one of which works in close association with the helicase to copy the leading-strand template in a continuous manner while the second copies the already unwound lagging-strand template in a discontinuous manner through the synthesis of Okazaki fragments. Considering that the lagging-strand polymerase has to recycle after the completion of every Okazaki fragment through the slow steps of primer synthesis and hand-off to the polymerase, it is not understood how the two strands are synthesized with the same net rate. Here we show, using the T7 replication proteins, that RNA primers are made 'on the fly' during ongoing DNA synthesis and that the leading-strand T7 replisome does not pause during primer synthesis, contrary to previous reports. Instead, the leading-strand polymerase remains limited by the speed of the helicase; it therefore synthesizes DNA more slowly than the lagging-strand polymerase. We show that the primase-helicase T7 gp4 maintains contact with the priming sequence during ongoing DNA synthesis; the nascent lagging-strand template therefore organizes into a priming loop that keeps the primer in physical proximity to the replication complex. Our findings provide three synergistic mechanisms of coordination: first, primers are made concomitantly with DNA synthesis; second, the priming loop ensures efficient primer use and hand-off to the polymerase; and third, the lagging-strand polymerase copies DNA faster, which allows it to keep up with leading-strand DNA synthesis overall.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896039/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896039/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pandey, Manjula -- Syed, Salman -- Donmez, Ilker -- Patel, Gayatri -- Ha, Taekjip -- Patel, Smita S -- GM065367/GM/NIGMS NIH HHS/ -- GM55310/GM/NIGMS NIH HHS/ -- R01 GM055310/GM/NIGMS NIH HHS/ -- R01 GM055310-14/GM/NIGMS NIH HHS/ -- R01 GM065367/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Dec 17;462(7275):940-3. doi: 10.1038/nature08611. Epub 2009 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19924126" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteriophage T7/*enzymology/genetics/*physiology ; DNA Primase/chemistry/metabolism ; DNA Replication/*physiology ; DNA, Viral/biosynthesis/metabolism ; DNA-Directed DNA Polymerase/chemistry/metabolism ; Fluorescence Resonance Energy Transfer ; Kinetics ; Models, Biological ; Multienzyme Complexes/chemistry/metabolism ; Protein Structure, Tertiary ; RNA/biosynthesis ; Time Factors
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    Telomerase modulates Wnt signalling by association with target gene chromatin (2009)
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    Publication Date: 2009-07-03
    Description: Stem cells are controlled, in part, by genetic pathways frequently dysregulated during human tumorigenesis. Either stimulation of Wnt/beta-catenin signalling or overexpression of telomerase is sufficient to activate quiescent epidermal stem cells in vivo, although the mechanisms by which telomerase exerts these effects are not understood. Here we show that telomerase directly modulates Wnt/beta-catenin signalling by serving as a cofactor in a beta-catenin transcriptional complex. The telomerase protein component TERT (telomerase reverse transcriptase) interacts with BRG1 (also called SMARCA4), a SWI/SNF-related chromatin remodelling protein, and activates Wnt-dependent reporters in cultured cells and in vivo. TERT serves an essential role in formation of the anterior-posterior axis in Xenopus laevis embryos, and this defect in Wnt signalling manifests as homeotic transformations in the vertebrae of Tert(-/-) mice. Chromatin immunoprecipitation of the endogenous TERT protein from mouse gastrointestinal tract shows that TERT physically occupies gene promoters of Wnt-dependent genes. These data reveal an unanticipated role for telomerase as a transcriptional modulator of the Wnt/beta-catenin signalling pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4349391/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4349391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Jae-Il -- Venteicher, Andrew S -- Hong, Ji Yeon -- Choi, Jinkuk -- Jun, Sohee -- Shkreli, Marina -- Chang, Woody -- Meng, Zhaojing -- Cheung, Peggie -- Ji, Hong -- McLaughlin, Margaret -- Veenstra, Timothy D -- Nusse, Roel -- McCrea, Pierre D -- Artandi, Steven E -- CA111691/CA/NCI NIH HHS/ -- CA125453/CA/NCI NIH HHS/ -- P30 CA124435/CA/NCI NIH HHS/ -- R01 CA111691/CA/NCI NIH HHS/ -- R01 CA125453/CA/NCI NIH HHS/ -- England -- Nature. 2009 Jul 2;460(7251):66-72. doi: 10.1038/nature08137.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19571879" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Choristoma/genetics/pathology ; Chromatin/*genetics ; DNA Helicases/metabolism ; Genes, Reporter/genetics ; HeLa Cells ; Humans ; Intestine, Small/metabolism ; Mice ; Nuclear Proteins/metabolism ; Oocytes/cytology/growth & development ; Plasmids/genetics ; Promoter Regions, Genetic/genetics ; *Signal Transduction ; Somites/abnormalities/embryology ; Telomerase/*metabolism ; Transcription Factors/metabolism ; Wnt Proteins/genetics/*metabolism ; Wnt3 Protein ; Xenopus laevis/embryology ; beta Catenin/genetics
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    Stem-cell inaction prompts concern (2009)
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    Publication Date: 2009-03-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wadman, Meredith -- England -- Nature. 2009 Feb 26;457(7233):1068. doi: 10.1038/4571068a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19256078" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryo Research/*economics/*legislation & jurisprudence ; *Embryonic Stem Cells ; *Federal Government ; Humans ; United States
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    Structure of a tetrameric MscL in an expanded intermediate state (2009)
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    Publication Date: 2009-08-25
    Description: The ability of cells to sense and respond to mechanical force underlies diverse processes such as touch and hearing in animals, gravitropism in plants, and bacterial osmoregulation. In bacteria, mechanosensation is mediated by the mechanosensitive channels of large (MscL), small (MscS), potassium-dependent (MscK) and mini (MscM) conductances. These channels act as 'emergency relief valves' protecting bacteria from lysis upon acute osmotic down-shock. Among them, MscL has been intensively studied since the original identification and characterization 15 years ago. MscL is reversibly and directly gated by changes in membrane tension. In the open state, MscL forms a non-selective 3 nS conductance channel which gates at tensions close to the lytic limit of the bacterial membrane. An earlier crystal structure at 3.5 A resolution of a pentameric MscL from Mycobacterium tuberculosis represents a closed-state or non-conducting conformation. MscL has a complex gating behaviour; it exhibits several intermediates between the closed and open states, including one putative non-conductive expanded state and at least three sub-conducting states. Although our understanding of the closed and open states of MscL has been increasing, little is known about the structures of the intermediate states despite their importance in elucidating the complete gating process of MscL. Here we present the crystal structure of a carboxy-terminal truncation mutant (Delta95-120) of MscL from Staphylococcus aureus (SaMscL(CDelta26)) at 3.8 A resolution. Notably, SaMscL(CDelta26) forms a tetrameric channel with both transmembrane helices tilted away from the membrane normal at angles close to that inferred for the open state, probably corresponding to a non-conductive but partially expanded intermediate state.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737600/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737600/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Zhenfeng -- Gandhi, Chris S -- Rees, Douglas C -- GM084211/GM/NIGMS NIH HHS/ -- R01 GM084211/GM/NIGMS NIH HHS/ -- R01 GM084211-01/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Sep 3;461(7260):120-4. doi: 10.1038/nature08277. Epub 2009 Aug 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, California 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19701184" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/*chemistry/metabolism ; Crystallography, X-Ray ; Ion Channel Gating ; Ion Channels/*chemistry/metabolism ; Models, Biological ; Models, Molecular ; Molecular Sequence Data ; Mycobacterium tuberculosis/chemistry/metabolism ; Pressure ; Protein Structure, Quaternary ; Staphylococcus aureus/*chemistry ; Structural Homology, Protein
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    Consent: criteria should be drawn up for tissue donors (2009)
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    Publication Date: 2009-10-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lo, Bernard -- Conklin, Bruce R -- England -- Nature. 2009 Oct 1;461(7264):593. doi: 10.1038/461593b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19794473" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cell Line ; Humans ; Informed Consent/*standards ; Male ; *Pluripotent Stem Cells/cytology/transplantation ; Testis/cytology ; *Tissue Donors
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    An oestrogen-receptor-alpha-bound human chromatin interactome (2009)
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    Publication Date: 2009-11-06
    Description: Genomes are organized into high-level three-dimensional structures, and DNA elements separated by long genomic distances can in principle interact functionally. Many transcription factors bind to regulatory DNA elements distant from gene promoters. Although distal binding sites have been shown to regulate transcription by long-range chromatin interactions at a few loci, chromatin interactions and their impact on transcription regulation have not been investigated in a genome-wide manner. Here we describe the development of a new strategy, chromatin interaction analysis by paired-end tag sequencing (ChIA-PET) for the de novo detection of global chromatin interactions, with which we have comprehensively mapped the chromatin interaction network bound by oestrogen receptor alpha (ER-alpha) in the human genome. We found that most high-confidence remote ER-alpha-binding sites are anchored at gene promoters through long-range chromatin interactions, suggesting that ER-alpha functions by extensive chromatin looping to bring genes together for coordinated transcriptional regulation. We propose that chromatin interactions constitute a primary mechanism for regulating transcription in mammalian genomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2774924/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2774924/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fullwood, Melissa J -- Liu, Mei Hui -- Pan, You Fu -- Liu, Jun -- Xu, Han -- Mohamed, Yusoff Bin -- Orlov, Yuriy L -- Velkov, Stoyan -- Ho, Andrea -- Mei, Poh Huay -- Chew, Elaine G Y -- Huang, Phillips Yao Hui -- Welboren, Willem-Jan -- Han, Yuyuan -- Ooi, Hong Sain -- Ariyaratne, Pramila N -- Vega, Vinsensius B -- Luo, Yanquan -- Tan, Peck Yean -- Choy, Pei Ye -- Wansa, K D Senali Abayratna -- Zhao, Bing -- Lim, Kar Sian -- Leow, Shi Chi -- Yow, Jit Sin -- Joseph, Roy -- Li, Haixia -- Desai, Kartiki V -- Thomsen, Jane S -- Lee, Yew Kok -- Karuturi, R Krishna Murthy -- Herve, Thoreau -- Bourque, Guillaume -- Stunnenberg, Hendrik G -- Ruan, Xiaoan -- Cacheux-Rataboul, Valere -- Sung, Wing-Kin -- Liu, Edison T -- Wei, Chia-Lin -- Cheung, Edwin -- Ruan, Yijun -- 1U54HG004557-01/HG/NHGRI NIH HHS/ -- R01 HG004456/HG/NHGRI NIH HHS/ -- R01 HG004456-01/HG/NHGRI NIH HHS/ -- R01 HG004456-02/HG/NHGRI NIH HHS/ -- R01 HG004456-03/HG/NHGRI NIH HHS/ -- R01HG003521-01/HG/NHGRI NIH HHS/ -- R01HG004456-01/HG/NHGRI NIH HHS/ -- U54 HG004557/HG/NHGRI NIH HHS/ -- U54 HG004557-01/HG/NHGRI NIH HHS/ -- U54 HG004557-02/HG/NHGRI NIH HHS/ -- U54 HG004557-03/HG/NHGRI NIH HHS/ -- U54 HG004557-04/HG/NHGRI NIH HHS/ -- England -- Nature. 2009 Nov 5;462(7269):58-64. doi: 10.1038/nature08497.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genome Institute of Singapore, Agency for Science, Technology and Research, Singapore 138672.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19890323" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Line ; Chromatin/*genetics/*metabolism ; Chromatin Immunoprecipitation ; Cross-Linking Reagents ; Estrogen Receptor alpha/*metabolism ; Formaldehyde ; Genome, Human/*genetics ; Humans ; Promoter Regions, Genetic/genetics ; Protein Binding ; Reproducibility of Results ; Sequence Analysis, DNA ; Transcription, Genetic ; Transcriptional Activation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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    Experimental evolution of bet hedging (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-11-06
    Description: Bet hedging-stochastic switching between phenotypic states-is a canonical example of an evolutionary adaptation that facilitates persistence in the face of fluctuating environmental conditions. Although bet hedging is found in organisms ranging from bacteria to humans, direct evidence for an adaptive origin of this behaviour is lacking. Here we report the de novo evolution of bet hedging in experimental bacterial populations. Bacteria were subjected to an environment that continually favoured new phenotypic states. Initially, our regime drove the successive evolution of novel phenotypes by mutation and selection; however, in two (of 12) replicates this trend was broken by the evolution of bet-hedging genotypes that persisted because of rapid stochastic phenotype switching. Genome re-sequencing of one of these switching types revealed nine mutations that distinguished it from the ancestor. The final mutation was both necessary and sufficient for rapid phenotype switching; nonetheless, the evolution of bet hedging was contingent upon earlier mutations that altered the relative fitness effect of the final mutation. These findings capture the adaptive evolution of bet hedging in the simplest of organisms, and suggest that risk-spreading strategies may have been among the earliest evolutionary solutions to life in fluctuating environments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beaumont, Hubertus J E -- Gallie, Jenna -- Kost, Christian -- Ferguson, Gayle C -- Rainey, Paul B -- England -- Nature. 2009 Nov 5;462(7269):90-3. doi: 10.1038/nature08504.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉New Zealand Institute for Advanced Study and Allan Wilson Centre for Molecular Ecology & Evolution, Massey University, Private Bag 102904, North Shore Mail Centre, North Shore City 0745, Auckland, New Zealand. h.j.e.beaumont@biology.leidenuniv.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19890329" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/genetics/*physiology ; *Biological Evolution ; Cell Shape ; Colony Count, Microbial ; *Environment ; Genes, Bacterial/genetics ; Genetic Fitness ; Genotype ; Models, Biological ; Phenotype ; Pseudomonas fluorescens/cytology/*genetics/growth & development/*physiology ; Selection, Genetic ; Stochastic Processes
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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