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  • Transcription, Genetic  (263)
  • American Association for the Advancement of Science (AAAS)  (263)
  • American Chemical Society (ACS)
  • American Geophysical Union (AGU)
  • Oxford University Press
  • 2010-2014  (112)
  • 1985-1989  (151)
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Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (263)
  • American Chemical Society (ACS)
  • American Geophysical Union (AGU)
  • Oxford University Press
  • Nature Publishing Group (NPG)  (59)
Years
Year
  • 1
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    The vigilante (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhattacharjee, Yudhijit -- New York, N.Y. -- Science. 2014 Mar 21;343(6177):1306-9. doi: 10.1126/science.343.6177.1306.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24653017" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Evolution ; DNA, Intergenic/genetics ; Databases, Nucleic Acid ; *Genome, Human ; *Genomics ; History, 20th Century ; History, 21st Century ; Humans ; Molecular Sequence Annotation ; Mutation ; National Human Genome Research Institute (U.S.) ; Transcription Factors/metabolism ; Transcription, Genetic ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Contribution of NAC transcription factors to plant adaptation to land (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-03-22
    Description: The development of cells specialized for water conduction or support is a striking innovation of plants that has enabled them to colonize land. The NAC transcription factors regulate the differentiation of these cells in vascular plants. However, the path by which plants with these cells have evolved from their nonvascular ancestors is unclear. We investigated genes of the moss Physcomitrella patens that encode NAC proteins. Loss-of-function mutants formed abnormal water-conducting and supporting cells, as well as malformed sporophyte cells, and overexpression induced ectopic differentiation of water-conducting-like cells. Our results show conservation of transcriptional regulation and cellular function between moss and Arabidopsis thaliana water-conducting cells. The conserved genetic basis suggests roles for NAC proteins in the adaptation of plants to land.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Bo -- Ohtani, Misato -- Yamaguchi, Masatoshi -- Toyooka, Kiminori -- Wakazaki, Mayumi -- Sato, Mayuko -- Kubo, Minoru -- Nakano, Yoshimi -- Sano, Ryosuke -- Hiwatashi, Yuji -- Murata, Takashi -- Kurata, Tetsuya -- Yoneda, Arata -- Kato, Ko -- Hasebe, Mitsuyasu -- Demura, Taku -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1505-8. doi: 10.1126/science.1248417. Epub 2014 Mar 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara 630-0192, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24652936" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/*genetics ; Amino Acid Sequence ; Arabidopsis/genetics/*physiology ; Bryopsida/genetics/*physiology ; *Gene Expression Regulation, Plant ; Genetic Loci ; Genome, Plant ; Molecular Sequence Data ; Plant Proteins/genetics/*physiology ; Plant Stems/growth & development ; Trans-Activators/genetics/*physiology ; Transcription, Genetic ; Water/*physiology
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  • 3
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    Synthetic biology. Genomically encoded analog memory with precise in vivo DNA writing in living cell populations (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-15
    Description: Cellular memory is crucial to many natural biological processes and sophisticated synthetic biology applications. Existing cellular memories rely on epigenetic switches or recombinases, which are limited in scalability and recording capacity. In this work, we use the DNA of living cell populations as genomic "tape recorders" for the analog and distributed recording of long-term event histories. We describe a platform for generating single-stranded DNA (ssDNA) in vivo in response to arbitrary transcriptional signals. When coexpressed with a recombinase, these intracellularly expressed ssDNAs target specific genomic DNA addresses, resulting in precise mutations that accumulate in cell populations as a function of the magnitude and duration of the inputs. This platform could enable long-term cellular recorders for environmental and biomedical applications, biological state machines, and enhanced genome engineering strategies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266475/" 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/PMC4266475/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farzadfard, Fahim -- Lu, Timothy K -- 1DP2OD008435/OD/NIH HHS/ -- 1P50GM098792/GM/NIGMS NIH HHS/ -- DP2 OD008435/OD/NIH HHS/ -- P50 GM098792/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Nov 14;346(6211):1256272. doi: 10.1126/science.1256272.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Synthetic Biology Group, Research Laboratory of Electronics, Department of Electrical Engineering and Computer Science and Department of Biological Engineering, Massachusetts Institute of Technology (MIT), 77 Massachusetts Avenue, Cambridge, MA 02139, USA. MIT Synthetic Biology Center, 500 Technology Square, Cambridge, MA 02139, USA. MIT Microbiology Program, 77 Massachusetts Avenue, Cambridge, MA 02139, USA. ; Synthetic Biology Group, Research Laboratory of Electronics, Department of Electrical Engineering and Computer Science and Department of Biological Engineering, Massachusetts Institute of Technology (MIT), 77 Massachusetts Avenue, Cambridge, MA 02139, USA. MIT Synthetic Biology Center, 500 Technology Square, Cambridge, MA 02139, USA. MIT Microbiology Program, 77 Massachusetts Avenue, Cambridge, MA 02139, USA. timlu@mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25395541" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *Bioengineering ; Cells ; DNA, Single-Stranded/*genetics ; Escherichia coli/genetics ; *Genetic Code ; Genomics/methods ; Information Storage and Retrieval/*methods ; Memory ; Molecular Sequence Data ; Synthetic Biology ; *Tape Recording ; Transcription, Genetic ; *Writing
    Print ISSN: 0036-8075
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  • 4
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    Life-span extension by a metacaspase in the yeast Saccharomyces cerevisiae (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-05-24
    Description: Single-cell species harbor ancestral structural homologs of caspase proteases, although the evolutionary benefit of such apoptosis-related proteins in unicellular organisms is unclear. Here, we found that the yeast metacaspase Mca1 is recruited to the insoluble protein deposit (IPOD) and juxtanuclear quality-control compartment (JUNQ) during aging and proteostatic stress. Elevating MCA1 expression counteracted accumulation of unfolded proteins and aggregates and extended life span in a heat shock protein Hsp104 disaggregase- and proteasome-dependent manner. Consistent with a role in protein quality control, genetic interaction analysis revealed that MCA1 buffers against deficiencies in the Hsp40 chaperone YDJ1 in a caspase cysteine-dependent manner. Life-span extension and aggregate management by Mca1 was only partly dependent on its conserved catalytic cysteine, which suggests that Mca1 harbors both caspase-dependent and independent functions related to life-span control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, Sandra Malmgren -- Hao, Xinxin -- Liu, Beidong -- Nystrom, Thomas -- New York, N.Y. -- Science. 2014 Jun 20;344(6190):1389-92. doi: 10.1126/science.1252634. Epub 2014 May 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Molecular Biology (CMB), University of Gothenburg, Medicinaregatan 9C, S-413 90 Goteborg, Sweden. ; Department of Chemistry and Molecular Biology (CMB), University of Gothenburg, Medicinaregatan 9C, S-413 90 Goteborg, Sweden. thomas.nystrom@cmb.gu.se beidong.liu@cmb.gu.se.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855027" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; Caspases/chemistry/genetics/*metabolism ; Catalysis ; Catalytic Domain ; Conserved Sequence ; Cysteine/chemistry/genetics ; Gene Expression Regulation, Fungal ; Heat-Shock Proteins/genetics/metabolism ; *Longevity ; Protein Transport ; *Proteolysis ; Saccharomyces cerevisiae/genetics/*physiology ; Saccharomyces cerevisiae Proteins/chemistry/genetics/*metabolism ; Transcription, Genetic ; Unfolded Protein Response
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 5
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    Detection of a recurrent DNAJB1-PRKACA chimeric transcript in fibrolamellar hepatocellular carcinoma (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-03-01
    Description: Fibrolamellar hepatocellular carcinoma (FL-HCC) is a rare liver tumor affecting adolescents and young adults with no history of primary liver disease or cirrhosis. We identified a chimeric transcript that is expressed in FL-HCC but not in adjacent normal liver and that arises as the result of a ~400-kilobase deletion on chromosome 19. The chimeric RNA is predicted to code for a protein containing the amino-terminal domain of DNAJB1, a homolog of the molecular chaperone DNAJ, fused in frame with PRKACA, the catalytic domain of protein kinase A. Immunoprecipitation and Western blot analyses confirmed that the chimeric protein is expressed in tumor tissue, and a cell culture assay indicated that it retains kinase activity. Evidence supporting the presence of the DNAJB1-PRKACA chimeric transcript in 100% of the FL-HCCs examined (15/15) suggests that this genetic alteration contributes to tumor pathogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286414/" 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/PMC4286414/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Honeyman, Joshua N -- Simon, Elana P -- Robine, Nicolas -- Chiaroni-Clarke, Rachel -- Darcy, David G -- Lim, Irene Isabel P -- Gleason, Caroline E -- Murphy, Jennifer M -- Rosenberg, Brad R -- Teegan, Lydia -- Takacs, Constantin N -- Botero, Sergio -- Belote, Rachel -- Germer, Soren -- Emde, Anne-Katrin -- Vacic, Vladimir -- Bhanot, Umesh -- LaQuaglia, Michael P -- Simon, Sanford M -- 2UL1RR024143/RR/NCRR NIH HHS/ -- UL1 RR024143/RR/NCRR NIH HHS/ -- UL1 TR000043/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Feb 28;343(6174):1010-4. doi: 10.1126/science.1249484.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular Biophysics, Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24578576" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinoma, Hepatocellular/enzymology/*genetics ; Chromosome Deletion ; Chromosomes, Human, Pair 19/genetics ; Cyclic AMP-Dependent Protein Kinase Catalytic Subunits/chemistry/*genetics ; Gene Expression Regulation, Neoplastic ; HSP40 Heat-Shock Proteins/chemistry/*genetics ; Humans ; Liver Neoplasms/enzymology/*genetics ; Oncogene Proteins, Fusion/*genetics ; Protein Multimerization ; Protein Structure, Tertiary ; Transcription, Genetic ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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  • 6
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    The robustness and evolvability of transcription factor binding sites (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-02-22
    Description: Robustness, the maintenance of a character in the presence of genetic change, can help preserve adaptive traits but also may hinder evolvability, the ability to bring forth novel adaptations. We used genotype networks to analyze the binding site repertoires of 193 transcription factors from mice and yeast, providing empirical evidence that robustness and evolvability need not be conflicting properties. Network vertices represent binding sites where two sites are connected if they differ in a single nucleotide. We show that the binding sites of larger genotype networks are not only more robust, but the sequences adjacent to such networks can also bind more transcription factors, thus demonstrating that robustness can facilitate evolvability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Payne, Joshua L -- Wagner, Andreas -- New York, N.Y. -- Science. 2014 Feb 21;343(6173):875-7. doi: 10.1126/science.1249046.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Zurich, Institute of Evolutionary Biology and Environmental Studies, Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24558158" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites/genetics ; Gene Regulatory Networks ; Mice ; Mutation ; Saccharomyces cerevisiae Proteins/chemistry ; Transcription Factors/*chemistry ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    MAVS, cGAS, and endogenous retroviruses in T-independent B cell responses (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-12-20
    Description: Multivalent molecules with repetitive structures including bacterial capsular polysaccharides and viral capsids elicit antibody responses through B cell receptor (BCR) crosslinking in the absence of T cell help. We report that immunization with these T cell-independent type 2 (TI-2) antigens causes up-regulation of endogenous retrovirus (ERV) RNAs in antigen-specific mouse B cells. These RNAs are detected via a mitochondrial antiviral signaling protein (MAVS)-dependent RNA sensing pathway or reverse-transcribed and detected via the cGAS-cGAMP-STING pathway, triggering a second, sustained wave of signaling that promotes specific immunoglobulin M production. Deficiency of both MAVS and cGAS, or treatment of MAVS-deficient mice with reverse transcriptase inhibitors, dramatically inhibits TI-2 antibody responses. These findings suggest that ERV and two innate sensing pathways that detect them are integral components of the TI-2 B cell signaling apparatus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391621/" 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/PMC4391621/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zeng, Ming -- Hu, Zeping -- Shi, Xiaolei -- Li, Xiaohong -- Zhan, Xiaoming -- Li, Xiao-Dong -- Wang, Jianhui -- Choi, Jin Huk -- Wang, Kuan-wen -- Purrington, Tiana -- Tang, Miao -- Fina, Maggy -- DeBerardinis, Ralph J -- Moresco, Eva Marie Y -- Pedersen, Gabriel -- McInerney, Gerald M -- Karlsson Hedestam, Gunilla B -- Chen, Zhijian J -- Beutler, Bruce -- P01 AI070167/AI/NIAID NIH HHS/ -- R01 AI093967/AI/NIAID NIH HHS/ -- R01 CA157996/CA/NCI NIH HHS/ -- U19 AI100627/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 19;346(6216):1486-92. doi: 10.1126/science.346.6216.1486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. ; Department of Pediatrics and Children's Medical Center Research Institute, and McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. ; Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. Howard Hughes Medical Institute, Department of Molecular Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9148, USA. ; Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Nobels vag 16, SE-171 77 Stockholm, Sweden. ; Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. Bruce.Beutler@UTSouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25525240" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/*immunology ; Animals ; Antibody Formation ; Antigens, T-Independent/*immunology ; B-Lymphocytes/*immunology ; Cytosol/immunology ; DNA/immunology ; Endogenous Retroviruses/genetics/*immunology ; Lymphocyte Activation ; Membrane Proteins/immunology ; Mice ; Mice, Inbred C57BL ; NF-kappa B/metabolism ; Nucleotides, Cyclic/immunology ; Nucleotidyltransferases/genetics/*immunology ; RNA, Viral/genetics/*immunology ; Transcription, Genetic
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  • 8
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    Synthetic biology. Programmable on-chip DNA compartments as artificial cells (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-08-16
    Description: The assembly of artificial cells capable of executing synthetic DNA programs has been an important goal for basic research and biotechnology. We assembled two-dimensional DNA compartments fabricated in silicon as artificial cells capable of metabolism, programmable protein synthesis, and communication. Metabolism is maintained by continuous diffusion of nutrients and products through a thin capillary, connecting protein synthesis in the DNA compartment with the environment. We programmed protein expression cycles, autoregulated protein levels, and a signaling expression gradient, equivalent to a morphogen, in an array of interconnected compartments at the scale of an embryo. Gene expression in the DNA compartment reveals a rich, dynamic system that is controlled by geometry, offering a means for studying biological networks outside a living cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karzbrun, Eyal -- Tayar, Alexandra M -- Noireaux, Vincent -- Bar-Ziv, Roy H -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):829-32. doi: 10.1126/science.1255550.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials and Interfaces, Weizmann Institute of Science, Rehovot 76100, Israel. ; Department of Physics, University of Minnesota, Minneapolis, MN 55455, USA. ; Department of Materials and Interfaces, Weizmann Institute of Science, Rehovot 76100, Israel. roy.bar-ziv@weizmann.ac.il.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124443" target="_blank"〉PubMed〈/a〉
    Keywords: Artificial Cells/*metabolism/ultrastructure ; *DNA/genetics/metabolism ; Diffusion ; *Gene Expression ; Gene Expression Regulation ; Gene Regulatory Networks ; Green Fluorescent Proteins/genetics/metabolism ; Kinetics ; Microfluidic Analytical Techniques ; Oligonucleotide Array Sequence Analysis ; Proteins/*metabolism ; Silicon ; Software ; Synthetic Biology/methods ; Templates, Genetic ; Transcription, Genetic
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  • 9
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    Stem cell signaling. An integral program for tissue renewal and regeneration: Wnt signaling and stem cell control (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-10-04
    Description: Stem cells fuel tissue development, renewal, and regeneration, and these activities are controlled by the local stem cell microenvironment, the "niche." Wnt signals emanating from the niche can act as self-renewal factors for stem cells in multiple mammalian tissues. Wnt proteins are lipid-modified, which constrains them to act as short-range cellular signals. The locality of Wnt signaling dictates that stem cells exiting the Wnt signaling domain differentiate, spatially delimiting the niche in certain tissues. In some instances, stem cells may act as or generate their own niche, enabling the self-organization of patterned tissues. In this Review, we discuss the various ways by which Wnt operates in stem cell control and, in doing so, identify an integral program for tissue renewal and regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clevers, Hans -- Loh, Kyle M -- Nusse, Roel -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Oct 3;346(6205):1248012. doi: 10.1126/science.1248012. Epub 2014 Oct 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW), University Medical Centre Utrecht and CancerGenomics.nl, 3584CT Utrecht, Netherlands. ; Department of Developmental Biology, Howard Hughes Medical Institute, Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA. ; Department of Developmental Biology, Howard Hughes Medical Institute, Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA. rnusse@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25278615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/physiology ; Cell Division ; Hair Follicle/physiology ; Humans ; Intestines/physiology ; Mammary Glands, Human/physiology ; Regeneration/genetics/*physiology ; Signal Transduction ; Stem Cell Niche/physiology ; Stem Cells/cytology/metabolism/*physiology ; Transcription, Genetic ; Wnt Proteins/*metabolism
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  • 10
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    Btk29A promotes Wnt4 signaling in the niche to terminate germ cell proliferation in Drosophila (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-01-18
    Description: Btk29A is the Drosophila ortholog of the mammalian Bruton's tyrosine kinase (Btk), mutations of which in humans cause a heritable immunodeficiency disease. Btk29A mutations stabilized the proliferating cystoblast fate, leading to an ovarian tumor. This phenotype was rescued by overexpression of wild-type Btk29A and phenocopied by the interference of Wnt4-beta-catenin signaling or its putative downstream nuclear protein Piwi in somatic escort cells. Btk29A and mammalian Btk directly phosphorylated tyrosine residues of beta-catenin, leading to the up-regulation of its transcriptional activity. Thus, we identify a transcriptional switch involving the kinase Btk29A/Btk and its phosphorylation target, beta-catenin, which functions downstream of Wnt4 in escort cells to terminate Drosophila germ cell proliferation through up-regulation of piwi expression. This signaling mechanism likely represents a versatile developmental switch.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamada-Kawaguchi, Noriko -- Nore, Beston F -- Kuwada, Yusuke -- Smith, C I Edvard -- Yamamoto, Daisuke -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):294-7. doi: 10.1126/science.1244512.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Neurosciences, Tohoku University Graduate School of Life Sciences, Sendai 980-8577, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436419" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins/*biosynthesis ; *Cell Proliferation ; DNA Breaks, Double-Stranded ; Drosophila Proteins/*biosynthesis/genetics/*metabolism ; Drosophila melanogaster/genetics/metabolism/*physiology ; Gene Knockdown Techniques ; Genomic Instability ; Germ Cells/cytology/metabolism/*physiology ; Glycoproteins/genetics/*metabolism ; Phosphorylation ; Protein-Tyrosine Kinases/genetics/*metabolism ; RNA, Small Interfering/genetics/metabolism ; Signal Transduction ; Transcription, Genetic ; Tyrosine/genetics/metabolism ; Up-Regulation ; Wnt Proteins/genetics/*metabolism ; beta Catenin/genetics/*metabolism
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  • 11
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    Convergent transcriptional specializations in the brains of humans and song-learning birds (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-12-17
    Description: Song-learning birds and humans share independently evolved similarities in brain pathways for vocal learning that are essential for song and speech and are not found in most other species. Comparisons of brain transcriptomes of song-learning birds and humans relative to vocal nonlearners identified convergent gene expression specializations in specific song and speech brain regions of avian vocal learners and humans. The strongest shared profiles relate bird motor and striatal song-learning nuclei, respectively, with human laryngeal motor cortex and parts of the striatum that control speech production and learning. Most of the associated genes function in motor control and brain connectivity. Thus, convergent behavior and neural connectivity for a complex trait are associated with convergent specialized expression of multiple genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4385736/" 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/PMC4385736/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfenning, Andreas R -- Hara, Erina -- Whitney, Osceola -- Rivas, Miriam V -- Wang, Rui -- Roulhac, Petra L -- Howard, Jason T -- Wirthlin, Morgan -- Lovell, Peter V -- Ganapathy, Ganeshkumar -- Mouncastle, Jacquelyn -- Moseley, M Arthur -- Thompson, J Will -- Soderblom, Erik J -- Iriki, Atsushi -- Kato, Masaki -- Gilbert, M Thomas P -- Zhang, Guojie -- Bakken, Trygve -- Bongaarts, Angie -- Bernard, Amy -- Lein, Ed -- Mello, Claudio V -- Hartemink, Alexander J -- Jarvis, Erich D -- DP1 OD000448/OD/NIH HHS/ -- R01 DC007218/DC/NIDCD NIH HHS/ -- R01DC007218/DC/NIDCD NIH HHS/ -- R21 DC007478/DC/NIDCD NIH HHS/ -- R24 GM092842/GM/NIGMS NIH HHS/ -- R24GM092842/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1256846. doi: 10.1126/science.1256846.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Howard Hughes Medical Institute, and Duke University Medical Center, Durham, NC 27710, USA. apfenning@csail.mit.edu amink@cs.duke.edu jarvis@neuro.duke.edu. ; Department of Neurobiology, Howard Hughes Medical Institute, and Duke University Medical Center, Durham, NC 27710, USA. ; Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, OR 97239, USA. ; Duke Proteomics and Metabolomics Core Facility, Center for Genomic and Computational Biology, Duke University Medical Center, Durham, NC 27710, USA. ; Laboratory for Symbolic Cognitive Development, Brain Science Institute, RIKEN, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, 1350 Copenhagen, Denmark. Trace and Environmental DNA Laboratory, Department of Environment and Agriculture, Curtin University, Perth, Western Australia 6102, Australia. ; China National GeneBank, BGI-Shenzhen, Shenzhen 518083, China. Centre for Social Evolution, Department of Biology, University of Copenhagen, DK-2100 Copenhagen, Denmark. ; Allen Institute for Brain Science, Seattle, WA 98103, USA. ; Department of Computer Science, Duke University, Durham, NC 27708, USA. apfenning@csail.mit.edu amink@cs.duke.edu jarvis@neuro.duke.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504733" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Birds/genetics/physiology ; Brain/anatomy & histology/*physiology ; Brain Mapping ; Corpus Striatum/anatomy & histology/physiology ; Evolution, Molecular ; Finches/*genetics/*physiology ; *Gene Expression Regulation ; Humans ; *Learning ; Male ; Motor Cortex/anatomy & histology/physiology ; Neural Pathways ; Species Specificity ; *Speech ; Transcription, Genetic ; *Transcriptome ; *Vocalization, Animal
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  • 12
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    An ancient defense system eliminates unfit cells from developing tissues during cell competition (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-12-06
    Description: Developing tissues that contain mutant or compromised cells present risks to animal health. Accordingly, the appearance of a population of suboptimal cells in a tissue elicits cellular interactions that prevent their contribution to the adult. Here we report that this quality control process, cell competition, uses specific components of the evolutionarily ancient and conserved innate immune system to eliminate Drosophila cells perceived as unfit. We find that Toll-related receptors (TRRs) and the cytokine Spatzle (Spz) lead to NFkappaB-dependent apoptosis. Diverse "loser" cells require different TRRs and NFkappaB factors and activate distinct pro-death genes, implying that the particular response is stipulated by the competitive context. Our findings demonstrate a functional repurposing of components of TRRs and NFkappaB signaling modules in the surveillance of cell fitness during development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, S N -- Amoyel, M -- Bergantinos, C -- de la Cova, C -- Schertel, C -- Basler, K -- Johnston, L A -- P40OD018537/OD/NIH HHS/ -- R01 GM078464/GM/NIGMS NIH HHS/ -- R01-GM084947/GM/NIGMS NIH HHS/ -- R21 HD067918/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2014 Dec 5;346(6214):1258236. doi: 10.1126/science.1258236.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland. ; Department of Genetics and Development, Columbia University, New York, NY 10032, USA. ; Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland. konrad.basler@imls.uzh.ch lj180@columbia.edu. ; Department of Genetics and Development, Columbia University, New York, NY 10032, USA. konrad.basler@imls.uzh.ch lj180@columbia.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25477468" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/genetics/*immunology ; Cell Communication/*immunology ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/cytology/genetics/growth & development ; Immunity, Innate/genetics/*immunology ; Mutation ; NF-kappa B/genetics/*metabolism ; Neuropeptides/genetics ; Toll-Like Receptors/genetics/*metabolism ; Transcription Factors/metabolism ; Transcription, Genetic
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  • 13
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    Poly-dipeptides encoded by the C9orf72 repeats bind nucleoli, impede RNA biogenesis, and kill cells (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-08-02
    Description: Many RNA regulatory proteins controlling pre-messenger RNA splicing contain serine:arginine (SR) repeats. Here, we found that these SR domains bound hydrogel droplets composed of fibrous polymers of the low-complexity domain of heterogeneous ribonucleoprotein A2 (hnRNPA2). Hydrogel binding was reversed upon phosphorylation of the SR domain by CDC2-like kinases 1 and 2 (CLK1/2). Mutated variants of the SR domains changing serine to glycine (SR-to-GR variants) also bound to hnRNPA2 hydrogels but were not affected by CLK1/2. When expressed in mammalian cells, these variants bound nucleoli. The translation products of the sense and antisense transcripts of the expansion repeats associated with the C9orf72 gene altered in neurodegenerative disease encode GRn and PRn repeat polypeptides. Both peptides bound to hnRNPA2 hydrogels independent of CLK1/2 activity. When applied to cultured cells, both peptides entered cells, migrated to the nucleus, bound nucleoli, and poisoned RNA biogenesis, which caused cell death.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459787/" 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/PMC4459787/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwon, Ilmin -- Xiang, Siheng -- Kato, Masato -- Wu, Leeju -- Theodoropoulos, Pano -- Wang, Tao -- Kim, Jiwoong -- Yun, Jonghyun -- Xie, Yang -- McKnight, Steven L -- U01 GM107623/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 5;345(6201):1139-45. doi: 10.1126/science.1254917. Epub 2014 Jul 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA. ; Quantitative Biomedical Research Center, Department of Clinical Sciences, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA. ; Department of Biochemistry, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA. steven.mcknight@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25081482" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amyotrophic Lateral Sclerosis/genetics/*metabolism/pathology ; Astrocytes/*metabolism/pathology ; Cell Death ; Cell Nucleolus/*metabolism ; Cells, Cultured ; Dipeptides/genetics/*metabolism/pharmacology ; Frontotemporal Dementia/genetics/*metabolism/pathology ; Glutamate Plasma Membrane Transport Proteins/genetics ; Heterogeneous-Nuclear Ribonucleoprotein Group A-B/*metabolism ; Humans ; Hydrogel ; Phosphorylation ; Protein Biosynthesis ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Proteins/*genetics ; RNA, Antisense/antagonists & inhibitors/biosynthesis ; RNA, Messenger/antagonists & inhibitors/biosynthesis ; RNA, Ribosomal/antagonists & inhibitors/biosynthesis ; Repetitive Sequences, Amino Acid ; Transcription, Genetic
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  • 14
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    Direct in vivo RNAi screen unveils myosin IIa as a tumor suppressor of squamous cell carcinomas (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-01-18
    Description: Mining modern genomics for cancer therapies is predicated on weeding out "bystander" alterations (nonconsequential mutations) and identifying "driver" mutations responsible for tumorigenesis and/or metastasis. We used a direct in vivo RNA interference (RNAi) strategy to screen for genes that upon repression predispose mice to squamous cell carcinomas (SCCs). Seven of our top hits-including Myh9, which encodes nonmuscle myosin IIa-have not been linked to tumor development, yet tissue-specific Myh9 RNAi and Myh9 knockout trigger invasive SCC formation on tumor-susceptible backgrounds. In human and mouse keratinocytes, myosin IIa's function is manifested not only in conventional actin-related processes but also in regulating posttranscriptional p53 stabilization. Myosin IIa is diminished in human SCCs with poor survival, which suggests that in vivo RNAi technology might be useful for identifying potent but low-penetrance tumor suppressors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159249/" 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/PMC4159249/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schramek, Daniel -- Sendoel, Ataman -- Segal, Jeremy P -- Beronja, Slobodan -- Heller, Evan -- Oristian, Daniel -- Reva, Boris -- Fuchs, Elaine -- R37 AR027883/AR/NIAMS NIH HHS/ -- R37-AR27883/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):309-13. doi: 10.1126/science.1248627.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Laboratory of Mammalian Cell Biology and Development, The Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436421" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Squamous Cell/*genetics/*pathology ; Genetic Testing ; Head and Neck Neoplasms/genetics/pathology ; Humans ; Lung Neoplasms/secondary ; Mice ; Mice, Knockout ; Molecular Motor Proteins/genetics/*physiology ; Mutation ; Myosin Heavy Chains/genetics/*physiology ; Nonmuscle Myosin Type IIA/genetics/*physiology ; RNA Interference ; Transcription, Genetic ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Proteins/genetics/*physiology
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  • 15
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    Convergent evolution of complex regulatory landscapes and pleiotropy at Hox loci (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-11-22
    Description: Hox genes are required during the morphogenesis of both vertebrate digits and external genitals. We investigated whether transcription in such distinct contexts involves a shared enhancer-containing landscape. We show that the same regulatory topology is used, yet with some tissue-specific enhancer-promoter interactions, suggesting the hijacking of a regulatory backbone from one context to the other. In addition, comparable organizations are observed at both HoxA and HoxD clusters, which separated through genome duplication in an ancestral invertebrate animal. We propose that this convergent regulatory evolution was triggered by the preexistence of some chromatin architecture, thus facilitating the subsequent recruitment of the appropriate transcription factors. Such regulatory topologies may have both favored and constrained the evolution of pleiotropic developmental loci in vertebrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lonfat, Nicolas -- Montavon, Thomas -- Darbellay, Fabrice -- Gitto, Sandra -- Duboule, Denis -- New York, N.Y. -- Science. 2014 Nov 21;346(6212):1004-6. doi: 10.1126/science.1257493.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Life Sciences, Ecole Polytechnique Federale de Lausanne, 1015 Lausanne, Switzerland. ; Department of Genetics and Evolution, University of Geneva, 1211 Geneva, Switzerland. ; School of Life Sciences, Ecole Polytechnique Federale de Lausanne, 1015 Lausanne, Switzerland. Department of Genetics and Evolution, University of Geneva, 1211 Geneva, Switzerland. denis.duboule@epfl.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25414315" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chick Embryo ; Enhancer Elements, Genetic ; *Evolution, Molecular ; Extremities ; *Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Genetic Loci/*genetics ; *Genetic Pleiotropy ; Genitalia/growth & development ; Homeodomain Proteins/*genetics ; Humans ; Mice ; Morphogenesis/*genetics ; Multigene Family ; Promoter Regions, Genetic ; Transcription, Genetic ; Vertebrates/genetics/*growth & development
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  • 16
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    Evolution. An epigenetic window into the past? (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-08-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Orlando, Ludovic -- Willerslev, Eske -- New York, N.Y. -- Science. 2014 Aug 1;345(6196):511-2. doi: 10.1126/science.1256515.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350K Copenhagen, Denmark. lorlando@snm.ku.dk. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350K Copenhagen, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25082684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Bone and Bones/chemistry/metabolism ; Chromatin/chemistry/metabolism ; *DNA Damage ; DNA Methylation ; *Epigenesis, Genetic ; Genome, Human ; Hair/chemistry/metabolism ; Humans ; Transcription, Genetic
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  • 17
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    Promoter architecture dictates cell-to-cell variability in gene expression (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-12-20
    Description: Variability in gene expression among genetically identical cells has emerged as a central preoccupation in the study of gene regulation; however, a divide exists between the predictions of molecular models of prokaryotic transcriptional regulation and genome-wide experimental studies suggesting that this variability is indifferent to the underlying regulatory architecture. We constructed a set of promoters in Escherichia coli in which promoter strength, transcription factor binding strength, and transcription factor copy numbers are systematically varied, and used messenger RNA (mRNA) fluorescence in situ hybridization to observe how these changes affected variability in gene expression. Our parameter-free models predicted the observed variability; hence, the molecular details of transcription dictate variability in mRNA expression, and transcriptional noise is specifically tunable and thus represents an evolutionarily accessible phenotypic parameter.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4388425/" 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/PMC4388425/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, Daniel L -- Brewster, Robert C -- Phillips, Rob -- 1 U54 CA143869/CA/NCI NIH HHS/ -- DP1 OD000217/OD/NIH HHS/ -- R01 GM085286/GM/NIGMS NIH HHS/ -- U54 CA143869/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2014 Dec 19;346(6216):1533-6. doi: 10.1126/science.1255301. Epub 2014 Dec 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Applied Physics, California Institute of Technology, Pasadena, CA 91125, USA. ; Department of Applied Physics, California Institute of Technology, Pasadena, CA 91125, USA. Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. ; Department of Applied Physics, California Institute of Technology, Pasadena, CA 91125, USA. Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. phillips@pboc.caltech.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25525251" target="_blank"〉PubMed〈/a〉
    Keywords: Cells/*metabolism ; DNA-Directed RNA Polymerases/metabolism ; Escherichia coli/genetics ; Gene Dosage ; *Gene Expression Regulation ; *Genetic Variation ; In Situ Hybridization ; Kinetics ; Lac Repressors/genetics/metabolism ; Models, Genetic ; *Promoter Regions, Genetic ; Protein Binding ; RNA, Messenger/genetics ; Transcription, Genetic
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  • 18
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    A long noncoding RNA mediates both activation and repression of immune response genes (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-08-03
    Description: An inducible program of inflammatory gene expression is central to antimicrobial defenses. This response is controlled by a collaboration involving signal-dependent activation of transcription factors, transcriptional co-regulators, and chromatin-modifying factors. We have identified a long noncoding RNA (lncRNA) that acts as a key regulator of this inflammatory response. Pattern recognition receptors such as the Toll-like receptors induce the expression of numerous lncRNAs. One of these, lincRNA-Cox2, mediates both the activation and repression of distinct classes of immune genes. Transcriptional repression of target genes is dependent on interactions of lincRNA-Cox2 with heterogeneous nuclear ribonucleoprotein A/B and A2/B1. Collectively, these studies unveil a central role of lincRNA-Cox2 as a broad-acting regulatory component of the circuit that controls the inflammatory response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376668/" 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/PMC4376668/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carpenter, Susan -- Aiello, Daniel -- Atianand, Maninjay K -- Ricci, Emiliano P -- Gandhi, Pallavi -- Hall, Lisa L -- Byron, Meg -- Monks, Brian -- Henry-Bezy, Meabh -- Lawrence, Jeanne B -- O'Neill, Luke A J -- Moore, Melissa J -- Caffrey, Daniel R -- Fitzgerald, Katherine A -- AI067497/AI/NIAID NIH HHS/ -- GM053234/GM/NIGMS NIH HHS/ -- R01 AI067497/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):789-92. doi: 10.1126/science.1240925. Epub 2013 Aug 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23907535" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Nucleus/metabolism ; Cyclooxygenase 2/genetics ; Cytokines/genetics/metabolism ; Cytosol/metabolism ; *Gene Expression Regulation ; Heterogeneous-Nuclear Ribonucleoproteins/metabolism ; Immunity, Innate/*genetics ; Inflammation/*genetics ; Macrophage Activation ; Macrophages/*immunology/*metabolism ; Mice ; Models, Immunological ; RNA Interference ; RNA, Long Noncoding/*genetics/metabolism ; Toll-Like Receptors/genetics/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; Transcriptional Activation
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  • 19
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    A histone mutant reproduces the phenotype caused by loss of histone-modifying factor Polycomb (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-02-09
    Description: Although many metazoan enzymes that add or remove specific modifications on histone proteins are essential transcriptional regulators, the functional significance of posttranslational modifications on histone proteins is not well understood. Here, we show in Drosophila that a point mutation in lysine 27 of histone H3 (H3-K27) fails to repress transcription of genes that are normally repressed by Polycomb repressive complex 2 (PRC2), the methyltransferase that modifies H3-K27. Moreover, differentiated H3-K27 mutant cells show homeotic transformations like those seen in PRC2 mutant cells. Taken together, these analyses demonstrate that H3-K27 is the crucial physiological substrate that PRC2 modifies for Polycomb repression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pengelly, Ana Raquel -- Copur, Omer -- Jackle, Herbert -- Herzig, Alf -- Muller, Jurg -- New York, N.Y. -- Science. 2013 Feb 8;339(6120):698-9. doi: 10.1126/science.1231382.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chromatin and Chromosome Biology Research Group, Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23393264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Drosophila Proteins/chemistry/*genetics/*metabolism ; Drosophila melanogaster/*genetics/growth & development/metabolism ; *Gene Expression Regulation ; Genes, Homeobox ; Genes, Insect ; Histones/chemistry/*genetics/*metabolism ; Lysine ; Mutant Proteins/chemistry/metabolism ; Nucleosomes/metabolism ; Phenotype ; Point Mutation ; Polycomb Repressive Complex 2/*metabolism ; Protein Processing, Post-Translational ; Transcription, Genetic ; Transgenes
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  • 20
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    Virology. Our viral inheritance (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiss, Robin A -- Stoye, Jonathan P -- MC_U117512710/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 May 17;340(6134):820-1. doi: 10.1126/science.1235148.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infection and Immunity, University College London, Gower Street, London WC1E 6BT, UK. rweiss@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23687035" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Viral/genetics ; Endogenous Retroviruses/*genetics ; Female ; Genome, Human/*genetics ; Humans ; Placenta/virology ; Pregnancy ; Promoter Regions, Genetic ; Proviruses/*genetics ; Transcription, Genetic
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    Bacterial subversion of host innate immune pathways (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-05-11
    Description: The pathogenesis of infection is a continuously evolving battle between the human host and the infecting microbe. The past decade has brought a burst of insights into the molecular mechanisms of innate immune responses to bacterial pathogens. In parallel, multiple specific mechanisms by which microorganisms subvert these host responses have been uncovered. This Review highlights recently characterized mechanisms by which bacterial pathogens avoid killing by innate host responses, including autophagy pathways and a proinflammatory cytokine transcriptional response, and by the manipulation of vesicular trafficking to avoid the toxicity of lysosomal enzymes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baxt, Leigh A -- Garza-Mayers, Anna Cristina -- Goldberg, Marcia B -- R01 AI081724/AI/NIAID NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 May 10;340(6133):697-701. doi: 10.1126/science.1235771.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Infectious Diseases, Massachusetts General Hospital, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23661751" target="_blank"〉PubMed〈/a〉
    Keywords: Autophagy/*immunology ; Bacteria/*immunology/pathogenicity ; Bacterial Infections/genetics/*immunology/microbiology ; Bacterial Secretion Systems ; Escherichia coli Proteins/metabolism ; Host-Pathogen Interactions/*immunology ; Humans ; *Immunity, Innate ; Inflammation/genetics/immunology/microbiology ; Phagocytosis ; Transcription, Genetic
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    Protein equilibration through somatic ring canals in Drosophila (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-05-25
    Description: Although intercellular bridges resulting from incomplete cytokinesis were discovered in somatic Drosophila tissues decades ago, the impact of these structures on intercellular communication and tissue biology is largely unknown. In this work, we demonstrate that the ~250-nanometer-diameter somatic ring canals permit diffusion of cytoplasmic contents between connected cells and across mitotic clone boundaries and enable the equilibration of protein between transcriptionally mosaic follicle cells in the Drosophila ovary. We obtained similar, although more restricted, results in the larval imaginal discs. Our work illustrates the lack of cytoplasmic autonomy in these tissues and suggests a role for somatic ring canals in promoting homogeneous protein expression within the tissue.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3819220/" 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/PMC3819220/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McLean, Peter F -- Cooley, Lynn -- GM043301/GM/NIGMS NIH HHS/ -- GM091791/GM/NIGMS NIH HHS/ -- P41 GM103313/GM/NIGMS NIH HHS/ -- R01 GM043301/GM/NIGMS NIH HHS/ -- RC1 GM091791/GM/NIGMS NIH HHS/ -- T32 GM007499/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Jun 21;340(6139):1445-7. doi: 10.1126/science.1234887. Epub 2013 May 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Yale School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23704373" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cytoplasm/*metabolism ; Cytoplasmic Structures/*metabolism/*ultrastructure ; Diffusion ; Drosophila ; Drosophila Proteins/*metabolism ; Female ; Giant Cells/ultrastructure ; Green Fluorescent Proteins/*metabolism ; Imaginal Discs/*metabolism/*ultrastructure ; Microscopy, Electron ; Mitosis ; Ovarian Follicle/cytology/metabolism/ultrastructure ; *Protein Transport ; Recombination, Genetic ; Transcription, Genetic ; Transgenes
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    Ezh2 orchestrates topographic migration and connectivity of mouse precerebellar neurons (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-01-12
    Description: We investigated the role of histone methyltransferase Ezh2 in tangential migration of mouse precerebellar pontine nuclei, the main relay between neocortex and cerebellum. By counteracting the sonic hedgehog pathway, Ezh2 represses Netrin1 in dorsal hindbrain, which allows normal pontine neuron migration. In Ezh2 mutants, ectopic Netrin1 derepression results in abnormal migration and supernumerary nuclei integrating in brain circuitry. Moreover, intrinsic topographic organization of pontine nuclei according to rostrocaudal progenitor origin is maintained throughout migration and correlates with patterned cortical input. Ezh2 maintains spatially restricted Hox expression, which, in turn, regulates differential expression of the repulsive receptor Unc5b in migrating neurons; together, they generate subsets with distinct responsiveness to environmental Netrin1. Thus, Ezh2-dependent epigenetic regulation of intrinsic and extrinsic transcriptional programs controls topographic neuronal guidance and connectivity in the cortico-ponto-cerebellar pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Meglio, Thomas -- Kratochwil, Claudius F -- Vilain, Nathalie -- Loche, Alberto -- Vitobello, Antonio -- Yonehara, Keisuke -- Hrycaj, Steven M -- Roska, Botond -- Peters, Antoine H F M -- Eichmann, Anne -- Wellik, Deneen -- Ducret, Sebastien -- Rijli, Filippo M -- T32 DK071212/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2013 Jan 11;339(6116):204-7. doi: 10.1126/science.1229326.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, 4058 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23307742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Movement ; Cerebellum/cytology/*embryology/metabolism ; Cerebral Cortex/embryology/physiology ; Epigenesis, Genetic ; Gene Expression Regulation, Developmental ; Genes, Homeobox ; Homeodomain Proteins/metabolism ; Metencephalon/embryology ; Mice ; Mice, Transgenic ; Nerve Growth Factors/genetics/metabolism ; Neural Pathways/*embryology/physiology ; Neurons/*physiology ; Polycomb Repressive Complex 2/genetics/*metabolism ; Pons/cytology/*embryology/metabolism ; Receptors, Cell Surface/genetics/metabolism ; Transcription, Genetic ; Tumor Suppressor Proteins/genetics/metabolism
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    Highly recurrent TERT promoter mutations in human melanoma (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-01-26
    Description: Systematic sequencing of human cancer genomes has identified many recurrent mutations in the protein-coding regions of genes but rarely in gene regulatory regions. Here, we describe two independent mutations within the core promoter of telomerase reverse transcriptase (TERT), the gene coding for the catalytic subunit of telomerase, which collectively occur in 50 of 70 (71%) melanomas examined. These mutations generate de novo consensus binding motifs for E-twenty-six (ETS) transcription factors, and in reporter assays, the mutations increased transcriptional activity from the TERT promoter by two- to fourfold. Examination of 150 cancer cell lines derived from diverse tumor types revealed the same mutations in 24 cases (16%), with preliminary evidence of elevated frequency in bladder and hepatocellular cancer cells. Thus, somatic mutations in regulatory regions of the genome may represent an important tumorigenic mechanism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4423787/" 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/PMC4423787/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Franklin W -- Hodis, Eran -- Xu, Mary Jue -- Kryukov, Gregory V -- Chin, Lynda -- Garraway, Levi A -- DP2 OD002750/OD/NIH HHS/ -- DP2OD002750/OD/NIH HHS/ -- R33 CA126674/CA/NCI NIH HHS/ -- R33CA126674/CA/NCI NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- T32GM07753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):957-9. doi: 10.1126/science.1229259. Epub 2013 Jan 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23348506" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Carcinoma, Hepatocellular/genetics ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; *Gene Expression Regulation, Neoplastic ; Humans ; Liver Neoplasms/genetics ; Melanoma/*genetics ; *Mutation ; *Promoter Regions, Genetic ; Proto-Oncogene Proteins c-ets/metabolism ; Telomerase/chemistry/*genetics/metabolism ; Transcription, Genetic
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    Circulating breast tumor cells exhibit dynamic changes in epithelial and mesenchymal composition (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-02-02
    Description: Epithelial-mesenchymal transition (EMT) of adherent epithelial cells to a migratory mesenchymal state has been implicated in tumor metastasis in preclinical models. To investigate its role in human cancer, we characterized EMT in circulating tumor cells (CTCs) from breast cancer patients. Rare primary tumor cells simultaneously expressed mesenchymal and epithelial markers, but mesenchymal cells were highly enriched in CTCs. Serial CTC monitoring in 11 patients suggested an association of mesenchymal CTCs with disease progression. In an index patient, reversible shifts between these cell fates accompanied each cycle of response to therapy and disease progression. Mesenchymal CTCs occurred as both single cells and multicellular clusters, expressing known EMT regulators, including transforming growth factor (TGF)-beta pathway components and the FOXC1 transcription factor. These data support a role for EMT in the blood-borne dissemination of human breast cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3760262/" 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/PMC3760262/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Min -- Bardia, Aditya -- Wittner, Ben S -- Stott, Shannon L -- Smas, Malgorzata E -- Ting, David T -- Isakoff, Steven J -- Ciciliano, Jordan C -- Wells, Marissa N -- Shah, Ajay M -- Concannon, Kyle F -- Donaldson, Maria C -- Sequist, Lecia V -- Brachtel, Elena -- Sgroi, Dennis -- Baselga, Jose -- Ramaswamy, Sridhar -- Toner, Mehmet -- Haber, Daniel A -- Maheswaran, Shyamala -- EB008047/EB/NIBIB NIH HHS/ -- K12 CA087723/CA/NCI NIH HHS/ -- NCI CA129933/CA/NCI NIH HHS/ -- R01 CA129933/CA/NCI NIH HHS/ -- U01 EB012493/EB/NIBIB NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Feb 1;339(6119):580-4. doi: 10.1126/science.1228522.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23372014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor/genetics/metabolism ; Breast Neoplasms/blood/genetics/*pathology ; Cell Count ; Cell Movement ; Epithelial Cells/pathology ; *Epithelial-Mesenchymal Transition ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mesoderm/pathology ; Mice ; Neoplasm Transplantation ; Neoplastic Cells, Circulating/metabolism/*pathology ; RNA, Neoplasm/chemistry/genetics ; Transcription, Genetic ; Transforming Growth Factor beta/genetics/metabolism
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    The Xist lncRNA exploits three-dimensional genome architecture to spread across the X chromosome (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-06
    Description: Many large noncoding RNAs (lncRNAs) regulate chromatin, but the mechanisms by which they localize to genomic targets remain unexplored. We investigated the localization mechanisms of the Xist lncRNA during X-chromosome inactivation (XCI), a paradigm of lncRNA-mediated chromatin regulation. During the maintenance of XCI, Xist binds broadly across the X chromosome. During initiation of XCI, Xist initially transfers to distal regions across the X chromosome that are not defined by specific sequences. Instead, Xist identifies these regions by exploiting the three-dimensional conformation of the X chromosome. Xist requires its silencing domain to spread across actively transcribed regions and thereby access the entire chromosome. These findings suggest a model in which Xist coats the X chromosome by searching in three dimensions, modifying chromosome structure, and spreading to newly accessible locations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3778663/" 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/PMC3778663/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Engreitz, Jesse M -- Pandya-Jones, Amy -- McDonel, Patrick -- Shishkin, Alexander -- Sirokman, Klara -- Surka, Christine -- Kadri, Sabah -- Xing, Jeffrey -- Goren, Alon -- Lander, Eric S -- Plath, Kathrin -- Guttman, Mitchell -- 1F32GM103139-01/GM/NIGMS NIH HHS/ -- DP5 OD012190/OD/NIH HHS/ -- DP5OD012190/OD/NIH HHS/ -- P01 GM099134/GM/NIGMS NIH HHS/ -- P01GM099134/GM/NIGMS NIH HHS/ -- P50HG006193/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):1237973. doi: 10.1126/science.1237973. Epub 2013 Jul 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23828888" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Chromatin/chemistry/metabolism ; Female ; *Genome ; Male ; Mice ; Models, Genetic ; RNA, Long Noncoding/chemistry/*metabolism ; Transcription, Genetic ; X Chromosome/*metabolism/ultrastructure ; *X Chromosome Inactivation
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    Mucus enhances gut homeostasis and oral tolerance by delivering immunoregulatory signals (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-09-28
    Description: A dense mucus layer in the large intestine prevents inflammation by shielding the underlying epithelium from luminal bacteria and food antigens. This mucus barrier is organized around the hyperglycosylated mucin MUC2. Here we show that the small intestine has a porous mucus layer, which permitted the uptake of MUC2 by antigen-sampling dendritic cells (DCs). Glycans associated with MUC2 imprinted DCs with anti-inflammatory properties by assembling a galectin-3-Dectin-1-FcgammaRIIB receptor complex that activated beta-catenin. This transcription factor interfered with DC expression of inflammatory but not tolerogenic cytokines by inhibiting gene transcription through nuclear factor kappaB. MUC2 induced additional conditioning signals in intestinal epithelial cells. Thus, mucus does not merely form a nonspecific physical barrier, but also constrains the immunogenicity of gut antigens by delivering tolerogenic signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005805/" 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/PMC4005805/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shan, Meimei -- Gentile, Maurizio -- Yeiser, John R -- Walland, A Cooper -- Bornstein, Victor U -- Chen, Kang -- He, Bing -- Cassis, Linda -- Bigas, Anna -- Cols, Montserrat -- Comerma, Laura -- Huang, Bihui -- Blander, J Magarian -- Xiong, Huabao -- Mayer, Lloyd -- Berin, Cecilia -- Augenlicht, Leonard H -- Velcich, Anna -- Cerutti, Andrea -- AI073899/AI/NIAID NIH HHS/ -- AI095245/AI/NIAID NIH HHS/ -- AI57653/AI/NIAID NIH HHS/ -- AI61093/AI/NIAID NIH HHS/ -- AI74378/AI/NIAID NIH HHS/ -- AI95613/AI/NIAID NIH HHS/ -- AI96187/AI/NIAID NIH HHS/ -- DK072201/DK/NIDDK NIH HHS/ -- P01 AI061093/AI/NIAID NIH HHS/ -- P01 DK072201/DK/NIDDK NIH HHS/ -- P60 DK020541/DK/NIDDK NIH HHS/ -- R01 AI057653/AI/NIAID NIH HHS/ -- R01 AI093577/AI/NIAID NIH HHS/ -- U01 AI095613/AI/NIAID NIH HHS/ -- U19 AI096187/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 25;342(6157):447-53. doi: 10.1126/science.1237910. Epub 2013 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24072822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dendritic Cells/immunology ; Galectin 3/genetics/metabolism ; Glycosylation ; *Homeostasis ; Humans ; Immune Tolerance/genetics/*immunology ; Inflammation/immunology ; Intestinal Mucosa/immunology ; Intestine, Small/*immunology ; Lectins, C-Type/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mouth/*immunology ; Mucin-2/genetics/physiology ; Mucus/*immunology ; NF-kappa B/metabolism ; Receptors, IgG/genetics/metabolism ; Transcription, Genetic ; beta Catenin/metabolism
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    Genome-wide quantitative enhancer activity maps identified by STARR-seq (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-01-19
    Description: Genomic enhancers are important regulators of gene expression, but their identification is a challenge, and methods depend on indirect measures of activity. We developed a method termed STARR-seq to directly and quantitatively assess enhancer activity for millions of candidates from arbitrary sources of DNA, which enables screens across entire genomes. When applied to the Drosophila genome, STARR-seq identifies thousands of cell type-specific enhancers across a broad continuum of strengths, links differential gene expression to differences in enhancer activity, and creates a genome-wide quantitative enhancer map. This map reveals the highly complex regulation of transcription, with several independent enhancers for both developmental regulators and ubiquitously expressed genes. STARR-seq can be used to identify and quantify enhancer activity in other eukaryotes, including humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arnold, Cosmas D -- Gerlach, Daniel -- Stelzer, Christoph -- Boryn, Lukasz M -- Rath, Martina -- Stark, Alexander -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1074-7. doi: 10.1126/science.1232542. Epub 2013 Jan 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology (IMP), Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23328393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping/*methods ; Drosophila melanogaster/genetics/growth & development ; Enhancer Elements, Genetic/*genetics ; Female ; *Gene Expression Regulation ; Gene Expression Regulation, Developmental ; Genome/genetics ; HeLa Cells ; Humans ; Ovary/metabolism ; Sequence Analysis, DNA ; Transcription, Genetic
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    Circadian control of chloroplast transcription by a nuclear-encoded timing signal (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-03-16
    Description: Circadian timekeeping in plants increases photosynthesis and productivity. There are circadian oscillations in the abundance of many chloroplast-encoded transcripts, but it is not known how the circadian clock regulates chloroplast transcription or the photosynthetic apparatus. We show that, in Arabidopsis, nuclear-encoded SIGMA FACTOR5 (SIG5) controls circadian rhythms of transcription of several chloroplast genes, revealing one pathway by which the nuclear-encoded circadian oscillator controls rhythms of chloroplast gene expression. We also show that SIG5 mediates the circadian gating of light input to a chloroplast-encoded gene. We have identified an evolutionarily conserved mechanism that communicates circadian timing information between organelles with distinct genetic systems and have established a new level of integration between eukaryotic circadian clocks and organelles of endosymbiotic origin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noordally, Zeenat B -- Ishii, Kenyu -- Atkins, Kelly A -- Wetherill, Sarah J -- Kusakina, Jelena -- Walton, Eleanor J -- Kato, Maiko -- Azuma, Miyuki -- Tanaka, Kan -- Hanaoka, Mitsumasa -- Dodd, Antony N -- BB/I005811/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Mar 15;339(6125):1316-9. doi: 10.1126/science.1230397.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉SynthSys, University of Edinburgh, Edinburgh, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23493713" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Arabidopsis/*genetics/*physiology ; Arabidopsis Proteins/genetics/*metabolism ; Cell Nucleus/metabolism ; Chloroplasts/*genetics ; *Circadian Rhythm ; *Gene Expression Regulation, Plant ; Photosystem II Protein Complex/metabolism ; Sigma Factor/genetics/*metabolism ; Transcription, Genetic
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    Neuroscience. Mapping neuronal diversity one cell at a time (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wichterle, Hynek -- Gifford, David -- Mazzoni, Esteban -- P01NS055923/NS/NINDS NIH HHS/ -- R01NS078097/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):726-7. doi: 10.1126/science.1235884.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Cell Biology, Columbia Stem Cell Initiative, Columbia University Medical Center, New York, NY 10032, USA. hw350@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23950522" target="_blank"〉PubMed〈/a〉
    Keywords: Central Nervous System/*cytology/physiology ; Electrophysiological Phenomena ; Gene Expression Profiling ; Humans ; Neurons/*classification/cytology/*physiology ; Phenotype ; *Single-Cell Analysis ; Transcription Factors/metabolism ; Transcription, Genetic ; Transcriptome
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    TERT promoter mutations in familial and sporadic melanoma (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-01-26
    Description: Cutaneous melanoma occurs in both familial and sporadic forms. We investigated a melanoma-prone family through linkage analysis and high-throughput sequencing and identified a disease-segregating germline mutation in the promoter of the telomerase reverse transcriptase (TERT) gene, which encodes the catalytic subunit of telomerase. The mutation creates a new binding motif for Ets transcription factors and ternary complex factors (TCFs) near the transcription start and, in reporter gene assays, caused up to twofold increase in transcription. We then screened the TERT promoter in sporadic melanoma and observed recurrent ultraviolet signature somatic mutations in 125 of 168 (74%) of human cell lines derived from metastatic melanomas, 45 of 53 corresponding metastatic tumor tissues (85%), and 25 of 77 (33%) primary melanomas. The majority of those mutations occurred at two positions in the TERT promoter and also generated binding motifs for Ets/TCF transcription factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horn, Susanne -- Figl, Adina -- Rachakonda, P Sivaramakrishna -- Fischer, Christine -- Sucker, Antje -- Gast, Andreas -- Kadel, Stephanie -- Moll, Iris -- Nagore, Eduardo -- Hemminki, Kari -- Schadendorf, Dirk -- Kumar, Rajiv -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):959-61. doi: 10.1126/science.1230062. Epub 2013 Jan 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Genetic Epidemiology, German Cancer Research Center, Im Neuenheimer Feld 580, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23348503" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Line, Tumor ; Female ; *Gene Expression Regulation, Neoplastic ; *Germ-Line Mutation ; High-Throughput Nucleotide Sequencing ; Humans ; Male ; Melanoma/*genetics/secondary ; Pedigree ; Polymorphism, Single Nucleotide ; *Promoter Regions, Genetic ; Proto-Oncogene Proteins c-ets/metabolism ; Sequence Analysis, DNA ; Skin Neoplasms/*genetics/pathology ; Telomerase/chemistry/*genetics/metabolism ; Transcription Initiation Site ; Transcription, Genetic ; ets-Domain Protein Elk-1/metabolism ; ets-Domain Protein Elk-4/metabolism
    Print ISSN: 0036-8075
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    Single-cell biology. Cells go solo. Introduction (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ray, L Bryan -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1187. doi: 10.1126/science.342.6163.1187.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311679" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells/*metabolism ; Mass Spectrometry ; Proteins/metabolism ; *Single-Cell Analysis ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Direct proteomic quantification of the secretome of activated immune cells (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-04-27
    Description: Protein secretion allows communication of distant cells in an organism and controls a broad range of physiological functions. We describe a quantitative, high-resolution mass spectrometric workflow to detect and quantify proteins that are released from immune cells upon receptor ligation. We quantified the time-resolved release of 775 proteins, including 52 annotated cytokines from only 150,000 primary Toll-like receptor 4-activated macrophages per condition. Achieving low picogram sensitivity, we detected secreted proteins whose abundance increased by a factor of more than 10,000 upon stimulation. Secretome to transcriptome comparisons revealed the transcriptionally decoupled release of lysosomal proteins. From genetic models, we defined secretory profiles that depended on distinct intracellular signaling adaptors and showed that secretion of many proinflammatory proteins is safeguarded by redundant mechanisms, whereas signaling adaptor synergy promoted the release of anti-inflammatory proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meissner, Felix -- Scheltema, Richard A -- Mollenkopf, Hans-Joachim -- Mann, Matthias -- New York, N.Y. -- Science. 2013 Apr 26;340(6131):475-8. doi: 10.1126/science.1232578.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23620052" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Lipopolysaccharides/immunology ; *Macrophage Activation ; Macrophages/*immunology ; Mass Spectrometry/*methods ; Mice ; Mice, Knockout ; Proteins/genetics/*secretion ; Proteome/genetics/*secretion ; Proteomics ; Toll-Like Receptor 4/*agonists ; Transcription, Genetic ; Transcriptome
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    Nuclear lamin-A scales with tissue stiffness and enhances matrix-directed differentiation (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-08-31
    Description: Tissues can be soft like fat, which bears little stress, or stiff like bone, which sustains high stress, but whether there is a systematic relationship between tissue mechanics and differentiation is unknown. Here, proteomics analyses revealed that levels of the nucleoskeletal protein lamin-A scaled with tissue elasticity, E, as did levels of collagens in the extracellular matrix that determine E. Stem cell differentiation into fat on soft matrix was enhanced by low lamin-A levels, whereas differentiation into bone on stiff matrix was enhanced by high lamin-A levels. Matrix stiffness directly influenced lamin-A protein levels, and, although lamin-A transcription was regulated by the vitamin A/retinoic acid (RA) pathway with broad roles in development, nuclear entry of RA receptors was modulated by lamin-A protein. Tissue stiffness and stress thus increase lamin-A levels, which stabilize the nucleus while also contributing to lineage determination.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3976548/" 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/PMC3976548/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Swift, Joe -- Ivanovska, Irena L -- Buxboim, Amnon -- Harada, Takamasa -- Dingal, P C Dave P -- Pinter, Joel -- Pajerowski, J David -- Spinler, Kyle R -- Shin, Jae-Won -- Tewari, Manorama -- Rehfeldt, Florian -- Speicher, David W -- Discher, Dennis E -- 8UL1TR000003/TR/NCATS NIH HHS/ -- CA010815/CA/NCI NIH HHS/ -- HL038794/HL/NHLBI NIH HHS/ -- P01DK032094/DK/NIDDK NIH HHS/ -- P30-DK090969/DK/NIDDK NIH HHS/ -- R01 EB007049/EB/NIBIB NIH HHS/ -- R01 HL062352/HL/NHLBI NIH HHS/ -- R01EB007049/EB/NIBIB NIH HHS/ -- R01HL062352/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 30;341(6149):1240104. doi: 10.1126/science.1240104.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biophysics Laboratory, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23990565" target="_blank"〉PubMed〈/a〉
    Keywords: Adipogenesis ; Animals ; *Cell Differentiation ; Collagen/analysis/chemistry/metabolism ; *Elasticity ; Extracellular Matrix/chemistry/metabolism ; Gene Expression Regulation, Developmental ; Humans ; Lamin Type A/chemistry/genetics/*metabolism ; Mesenchymal Stromal Cells/*cytology ; Mice ; Models, Biological ; Nuclear Lamina/metabolism ; *Osteogenesis/genetics ; Protein Conformation ; Proteome ; *Stress, Mechanical ; Transcription, Genetic ; Tretinoin/metabolism ; Vitamin A/metabolism
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    Meiosis-specific noncoding RNA mediates robust pairing of homologous chromosomes in meiosis (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-05-15
    Description: Pairing and recombination of homologous chromosomes are essential for ensuring reductional segregation in meiosis. However, the mechanisms by which chromosomes recognize their homologous partners are poorly understood. Here, we report that the sme2 gene encodes a meiosis-specific noncoding RNA that mediates homologous recognition in the fission yeast Schizosaccharomyces pombe. The sme2 locus shows robust pairing from early in meiotic prophase. The sme2 RNA transcripts accumulate at their respective gene loci and greatly enhance pairing of homologous loci: Deletion of the sme2 sequence eliminates this robust pairing, whereas transposition to other chromosomal sites confers robust pairing at those ectopic sites. Thus, we propose that RNA transcripts retained on the chromosome play an active role in recognition of homologous chromosomes for pairing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, Da-Qiao -- Okamasa, Kasumi -- Yamane, Miho -- Tsutsumi, Chihiro -- Haraguchi, Tokuko -- Yamamoto, Masayuki -- Hiraoka, Yasushi -- New York, N.Y. -- Science. 2012 May 11;336(6082):732-6. doi: 10.1126/science.1219518.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Advanced ICT Research Institute Kobe, National Institute of Information and Communications Technology, Kobe 651-2492, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22582262" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Pairing ; Chromosomes, Fungal/*physiology ; Genes, Fungal ; *Meiosis ; Models, Genetic ; Prophase ; RNA, Fungal/genetics ; RNA, Untranslated/*genetics ; RNA-Binding Proteins/genetics/metabolism ; Recombination, Genetic ; Schizosaccharomyces/*genetics/physiology ; Schizosaccharomyces pombe Proteins/genetics/metabolism ; Telomere/physiology ; Transcription, Genetic ; mRNA Cleavage and Polyadenylation Factors/genetics
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    MARF1 regulates essential oogenic processes in mice (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-03-24
    Description: Development of fertilization-competent oocytes depends on integrated processes controlling meiosis, cytoplasmic development, and maintenance of genomic integrity. We show that meiosis arrest female 1 (MARF1) is required for these processes in mammalian oocytes. Mutations of Marf1 cause female infertility characterized by up-regulation of a cohort of transcripts, increased retrotransposon expression, defective cytoplasmic maturation, and meiotic arrest. Up-regulation of protein phosphatase 2 catalytic subunit (PPP2CB) is key to the meiotic arrest phenotype. Moreover, Iap and Line1 retrotransposon messenger RNAs are also up-regulated, and, concomitantly, DNA double-strand breaks are elevated in mutant oocytes. Therefore MARF1, by suppressing levels of specific transcripts, is an essential regulator of important oogenic processes leading to female fertility and the development of healthy offspring.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612990/" 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/PMC3612990/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, You-Qiang -- Sugiura, Koji -- Sun, Fengyun -- Pendola, Janice K -- Cox, Gregory A -- Handel, Mary Ann -- Schimenti, John C -- Eppig, John J -- CA34196/CA/NCI NIH HHS/ -- HD42137/HD/NICHD NIH HHS/ -- P01 HD042137/HD/NICHD NIH HHS/ -- P30 CA034196/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1496-9. doi: 10.1126/science.1214680.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Jackson Laboratory, Bar Harbor, ME 04609, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22442484" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Cycle Proteins/chemistry/genetics/*metabolism ; DNA Breaks, Double-Stranded ; Embryonic Development ; Female ; *Fertility ; Meiosis ; Mice ; Molecular Sequence Data ; Mutation ; Oocytes/*physiology ; *Oogenesis ; Phenotype ; Protein Phosphatase 2/genetics/metabolism ; Protein Structure, Tertiary ; RNA, Messenger/genetics/metabolism ; Retroelements ; Transcription, Genetic ; Transcriptome ; Up-Regulation
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    The structure of native influenza virion ribonucleoproteins (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-11-28
    Description: The influenza viruses cause annual epidemics of respiratory disease and occasional pandemics, which constitute a major public-health issue. The segmented negative-stranded RNAs are associated with the polymerase complex and nucleoprotein (NP), forming ribonucleoproteins (RNPs), which are responsible for virus transcription and replication. We describe the structure of native RNPs derived from virions. They show a double-helical conformation in which two NP strands of opposite polarity are associated with each other along the helix. Both strands are connected by a short loop at one end of the particle and interact with the polymerase complex at the other end. This structure will be relevant for unraveling the mechanisms of nuclear import of parental virus RNPs, their transcription and replication, and the encapsidation of progeny RNPs into virions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arranz, Rocio -- Coloma, Rocio -- Chichon, Francisco Javier -- Conesa, Jose Javier -- Carrascosa, Jose L -- Valpuesta, Jose M -- Ortin, Juan -- Martin-Benito, Jaime -- New York, N.Y. -- Science. 2012 Dec 21;338(6114):1634-7. doi: 10.1126/science.1228172. Epub 2012 Nov 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Macromolecular Structure, Centro Nacional de Biotecnologia [Consejo Superior de Investigaciones Cienficas (CSIC)], Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23180776" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/metabolism/virology ; Cryoelectron Microscopy ; Electron Microscope Tomography ; Image Processing, Computer-Assisted ; Influenza A Virus, H1N1 Subtype/*chemistry/physiology/ultrastructure ; Madin Darby Canine Kidney Cells ; Microscopy, Electron ; Models, Molecular ; Protein Conformation ; Protein Structure, Secondary ; RNA Replicase/chemistry/metabolism/ultrastructure ; RNA, Viral/*chemistry/metabolism ; RNA-Binding Proteins/chemistry/metabolism/ultrastructure ; Ribonucleoproteins/*chemistry/metabolism/ultrastructure ; Transcription, Genetic ; Viral Core Proteins/chemistry/metabolism/ultrastructure ; Viral Proteins/*chemistry/metabolism/ultrastructure ; Virion/*chemistry/ultrastructure
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    Mapping the core of the Arabidopsis circadian clock defines the network structure of the oscillator (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-03-10
    Description: In many organisms, the circadian clock is composed of functionally coupled morning and evening oscillators. In Arabidopsis, oscillator coupling relies on a core loop in which the evening oscillator component TIMING OF CAB EXPRESSION 1 (TOC1) was proposed to activate a subset of morning-expressed oscillator genes. Here, we show that TOC1 does not function as an activator but rather as a general repressor of oscillator gene expression. Repression occurs through TOC1 rhythmic association to the promoters of the oscillator genes. Hormone-dependent induction of TOC1 and analysis of RNA interference plants show that TOC1 prevents the activation of morning-expressed genes at night. Our study overturns the prevailing model of the Arabidopsis circadian clock, showing that the morning and evening oscillator loops are connected through the repressing activity of TOC1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, W -- Perez-Garcia, P -- Pokhilko, A -- Millar, A J -- Antoshechkin, I -- Riechmann, J L -- Mas, P -- BB/D019621/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- D019621/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Apr 6;336(6077):75-9. doi: 10.1126/science.1219075. Epub 2012 Mar 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Research in Agricultural Genomics, Barcelona 08193, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22403178" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/*physiology ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Chromatin Immunoprecipitation ; *Circadian Clocks/genetics ; DNA-Binding Proteins/genetics/metabolism ; Darkness ; Dexamethasone/pharmacology ; Feedback, Physiological ; *Gene Expression Regulation, Plant ; Genes, Plant ; Light ; Photoperiod ; Plants, Genetically Modified ; Promoter Regions, Genetic ; RNA Interference ; Repressor Proteins/genetics/*metabolism ; Transcription Factors/chemistry/genetics/*metabolism ; Transcription, Genetic
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    Regional astrocyte allocation regulates CNS synaptogenesis and repair (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-30
    Description: Astrocytes, the most abundant cell population in the central nervous system (CNS), are essential for normal neurological function. We show that astrocytes are allocated to spatial domains in mouse spinal cord and brain in accordance with their embryonic sites of origin in the ventricular zone. These domains remain stable throughout life without evidence of secondary tangential migration, even after acute CNS injury. Domain-specific depletion of astrocytes in ventral spinal cord resulted in abnormal motor neuron synaptogenesis, which was not rescued by immigration of astrocytes from adjoining regions. Our findings demonstrate that region-restricted astrocyte allocation is a general CNS phenomenon and reveal intrinsic limitations of the astroglial response to injury.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4059181/" 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/PMC4059181/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Hui-Hsin -- Li, Huiliang -- Fuentealba, Luis C -- Molofsky, Anna V -- Taveira-Marques, Raquel -- Zhuang, Helin -- Tenney, April -- Murnen, Alice T -- Fancy, Stephen P J -- Merkle, Florian -- Kessaris, Nicoletta -- Alvarez-Buylla, Arturo -- Richardson, William D -- Rowitch, David H -- G0501173/Medical Research Council/United Kingdom -- G0800575/Medical Research Council/United Kingdom -- R01 NS028478/NS/NINDS NIH HHS/ -- R37 HD032116/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jul 20;337(6092):358-62. doi: 10.1126/science.1222381. Epub 2012 Jun 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745251" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*physiology ; Bacterial Proteins/metabolism ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Brain/abnormalities/*cytology/physiology ; Brain Injuries/physiopathology ; *Cell Movement ; Green Fluorescent Proteins ; Homeodomain Proteins/metabolism ; Integrases/genetics ; Luminescent Proteins/metabolism ; Mice ; Mice, Transgenic ; Motor Neurons/*physiology ; Nerve Tissue Proteins/genetics ; Proteins/metabolism ; RNA, Untranslated ; Spinal Cord/abnormalities/*cytology/physiology ; Spinal Cord Injuries/physiopathology ; Synapses/*physiology ; Transcription Factors/metabolism ; Transcription, Genetic
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    Global gene deletion analysis exploring yeast filamentous growth (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-09-18
    Description: The dimorphic switch from a single-cell budding yeast to a filamentous form enables Saccharomyces cerevisiae to forage for nutrients and the opportunistic pathogen Candida albicans to invade human tissues and evade the immune system. We constructed a genome-wide set of targeted deletion alleles and introduced them into a filamentous S. cerevisiae strain, Sigma1278b. We identified genes involved in morphologically distinct forms of filamentation: haploid invasive growth, biofilm formation, and diploid pseudohyphal growth. Unique genes appear to underlie each program, but we also found core genes with general roles in filamentous growth, including MFG1 (YDL233w), whose product binds two morphogenetic transcription factors, Flo8 and Mss11, and functions as a critical transcriptional regulator of filamentous growth in both S. cerevisiae and C. albicans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, Owen -- Shapiro, Rebecca S -- Kurat, Christoph F -- Mayhew, David -- Baryshnikova, Anastasia -- Chin, Brian -- Lin, Zhen-Yuan -- Cox, Michael J -- Vizeacoumar, Frederick -- Cheung, Doris -- Bahr, Sondra -- Tsui, Kyle -- Tebbji, Faiza -- Sellam, Adnane -- Istel, Fabian -- Schwarzmuller, Tobias -- Reynolds, Todd B -- Kuchler, Karl -- Gifford, David K -- Whiteway, Malcolm -- Giaever, Guri -- Nislow, Corey -- Costanzo, Michael -- Gingras, Anne-Claude -- Mitra, Robi David -- Andrews, Brenda -- Fink, Gerald R -- Cowen, Leah E -- Boone, Charles -- 42516-4/Canadian Institutes of Health Research/Canada -- GM035010/GM/NIGMS NIH HHS/ -- GM40266/GM/NIGMS NIH HHS/ -- MOP-97939/Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Sep 14;337(6100):1353-6. doi: 10.1126/science.1224339.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Banting and Best Department of Medical Research, University of Toronto, Toronto, ON M5S 3E1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22984072" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Biofilms/growth & development ; Candida albicans/cytology/*genetics/*growth & development ; DNA Mutational Analysis ; Gene Deletion ; *Gene Expression Regulation, Fungal ; Hyphae/genetics/growth & development ; Nuclear Proteins/genetics ; Saccharomyces cerevisiae/cytology/*genetics/*growth & development ; Saccharomyces cerevisiae Proteins/genetics ; Trans-Activators/genetics ; Transcription Factors/genetics ; Transcription, Genetic
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    Using gene expression noise to understand gene regulation (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-14
    Description: Phenotypic variation is ubiquitous in biology and is often traceable to underlying genetic and environmental variation. However, even genetically identical cells in identical environments display variable phenotypes. Stochastic gene expression, or gene expression "noise," has been suggested as a major source of this variability, and its physiological consequences have been topics of intense research for the last decade. Several recent studies have measured variability in protein and messenger RNA levels, and they have discovered strong connections between noise and gene regulation mechanisms. When integrated with discrete stochastic models, measurements of cell-to-cell variability provide a sensitive "fingerprint" with which to explore fundamental questions of gene regulation. In this review, we highlight several studies that used gene expression variability to develop a quantitative understanding of the mechanisms and dynamics of gene regulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3358231/" 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/PMC3358231/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Munsky, Brian -- Neuert, Gregor -- van Oudenaarden, Alexander -- 1DP1OD003936/OD/NIH HHS/ -- DP1 CA174420/CA/NCI NIH HHS/ -- DP1 OD003936/OD/NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 13;336(6078):183-7. doi: 10.1126/science.1216379.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Nonlinear Studies, the National Flow Cytometry Resource, Los Alamos National Laboratory, Los Alamos, NM 87545, USA. munsky@lanl.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22499939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Gene Expression ; *Gene Expression Regulation ; Humans ; *Models, Genetic ; Models, Statistical ; Phenotype ; RNA, Messenger/genetics/metabolism ; Stochastic Processes ; Transcription, Genetic
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    American Chemical Society Spring Meeting. New genetic letters augment DNA, and soon perhaps life (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-04-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, Robert F -- New York, N.Y. -- Science. 2012 Apr 20;336(6079):292-3. doi: 10.1126/science.336.6079.292-c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22517838" target="_blank"〉PubMed〈/a〉
    Keywords: DNA/*chemistry/*metabolism ; *Genetic Code ; Nucleotides/chemical synthesis/*chemistry/*metabolism ; Protein Biosynthesis ; Transcription, Genetic
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    Drosophila dosage compensation involves enhanced Pol II recruitment to male X-linked promoters (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-07-24
    Description: Through hyperacetylation of histone H4 lysine 16 (H4K16), the male-specific lethal (MSL) complex in Drosophila approximately doubles transcription from the single male X chromosome in order to match X-linked expression in females and expression from diploid autosomes. By obtaining accurate measurements of RNA polymerase II (Pol II) occupancies and short promoter-proximal RNA production, we detected a consistent, genome-scale increase in Pol II activity at the promoters of male X-linked genes. Moreover, we found that enhanced Pol II recruitment to male X-linked promoters is largely dependent on the MSL complex. These observations provide insights into how global modulation of chromatin structure by histone acetylation contributes to the precise control of Pol II function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conrad, Thomas -- Cavalli, Florence M G -- Vaquerizas, Juan M -- Luscombe, Nicholas M -- Akhtar, Asifa -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2012 Aug 10;337(6095):742-6. doi: 10.1126/science.1221428. Epub 2012 Jul 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg im Breisgau, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22821985" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Cell Line ; Chromatin Immunoprecipitation ; DNA Polymerase II/*metabolism ; *Dosage Compensation, Genetic ; Drosophila/*genetics/metabolism ; Drosophila Proteins/*metabolism ; Female ; Genes, Insect ; *Genes, X-Linked ; Histones/metabolism ; Male ; Multigene Family ; *Promoter Regions, Genetic ; Sex Characteristics ; Transcription, Genetic ; X Chromosome/*genetics
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    Decoding human cytomegalovirus (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-11-28
    Description: The human cytomegalovirus (HCMV) genome was sequenced 20 years ago. However, like those of other complex viruses, our understanding of its protein coding potential is far from complete. We used ribosome profiling and transcript analysis to experimentally define the HCMV translation products and follow their temporal expression. We identified hundreds of previously unidentified open reading frames and confirmed a fraction by means of mass spectrometry. We found that regulated use of alternative transcript start sites plays a broad role in enabling tight temporal control of HCMV protein expression and allowing multiple distinct polypeptides to be generated from a single genomic locus. Our results reveal an unanticipated complexity to the HCMV coding capacity and illustrate the role of regulated changes in transcript start sites in generating this complexity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3817102/" 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/PMC3817102/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stern-Ginossar, Noam -- Weisburd, Ben -- Michalski, Annette -- Le, Vu Thuy Khanh -- Hein, Marco Y -- Huang, Sheng-Xiong -- Ma, Ming -- Shen, Ben -- Qian, Shu-Bing -- Hengel, Hartmut -- Mann, Matthias -- Ingolia, Nicholas T -- Weissman, Jonathan S -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 23;338(6110):1088-93. doi: 10.1126/science.1227919.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, Howard Hughes Medical Institute, University of California, San Francisco, San Francisico, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23180859" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Cytomegalovirus/*genetics ; Cytomegalovirus Infections/*virology ; Genetic Variation ; *Genome, Viral ; Humans ; *Open Reading Frames ; Protein Biosynthesis/genetics ; Proteome/genetics ; Sequence Analysis, DNA ; Transcription, Genetic
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    Quantitative sequencing of 5-methylcytosine and 5-hydroxymethylcytosine at single-base resolution (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-04-28
    Description: 5-Methylcytosine can be converted to 5-hydroxymethylcytosine (5hmC) in mammalian DNA by the ten-eleven translocation (TET) enzymes. We introduce oxidative bisulfite sequencing (oxBS-Seq), the first method for quantitative mapping of 5hmC in genomic DNA at single-nucleotide resolution. Selective chemical oxidation of 5hmC to 5-formylcytosine (5fC) enables bisulfite conversion of 5fC to uracil. We demonstrate the utility of oxBS-Seq to map and quantify 5hmC at CpG islands (CGIs) in mouse embryonic stem (ES) cells and identify 800 5hmC-containing CGIs that have on average 3.3% hydroxymethylation. High levels of 5hmC were found in CGIs associated with transcriptional regulators and in long interspersed nuclear elements, suggesting that these regions might undergo epigenetic reprogramming in ES cells. Our results open new questions on 5hmC dynamics and sequence-specific targeting by TETs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Booth, Michael J -- Branco, Miguel R -- Ficz, Gabriella -- Oxley, David -- Krueger, Felix -- Reik, Wolf -- Balasubramanian, Shankar -- 095645/Wellcome Trust/United Kingdom -- 11961/Cancer Research UK/United Kingdom -- G0801156/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 May 18;336(6083):934-7. doi: 10.1126/science.1220671. Epub 2012 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Cambridge, Cambridge CB2 1EW, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22539555" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/*analysis ; Animals ; *CpG Islands ; Cytosine/*analogs & derivatives/analysis/chemistry ; DNA/*chemistry/genetics ; DNA Methylation ; *Embryonic Stem Cells/physiology ; Epigenesis, Genetic ; Genes, Intracisternal A-Particle ; High-Throughput Nucleotide Sequencing ; Long Interspersed Nucleotide Elements ; Mice ; Oxidation-Reduction ; Rhenium/chemistry ; *Sequence Analysis, DNA ; Sulfites ; Transcription, Genetic ; Uracil/chemistry
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    Suppression of oxidative stress by beta-hydroxybutyrate, an endogenous histone deacetylase inhibitor (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-12-12
    Description: Concentrations of acetyl-coenzyme A and nicotinamide adenine dinucleotide (NAD(+)) affect histone acetylation and thereby couple cellular metabolic status and transcriptional regulation. We report that the ketone body d-beta-hydroxybutyrate (betaOHB) is an endogenous and specific inhibitor of class I histone deacetylases (HDACs). Administration of exogenous betaOHB, or fasting or calorie restriction, two conditions associated with increased betaOHB abundance, all increased global histone acetylation in mouse tissues. Inhibition of HDAC by betaOHB was correlated with global changes in transcription, including that of the genes encoding oxidative stress resistance factors FOXO3A and MT2. Treatment of cells with betaOHB increased histone acetylation at the Foxo3a and Mt2 promoters, and both genes were activated by selective depletion of HDAC1 and HDAC2. Consistent with increased FOXO3A and MT2 activity, treatment of mice with betaOHB conferred substantial protection against oxidative stress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/" 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/PMC3735349/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimazu, Tadahiro -- Hirschey, Matthew D -- Newman, John -- He, Wenjuan -- Shirakawa, Kotaro -- Le Moan, Natacha -- Grueter, Carrie A -- Lim, Hyungwook -- Saunders, Laura R -- Stevens, Robert D -- Newgard, Christopher B -- Farese, Robert V Jr -- de Cabo, Rafael -- Ulrich, Scott -- Akassoglou, Katerina -- Verdin, Eric -- P30 DK026743/DK/NIDDK NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- R01 DK056084/DK/NIDDK NIH HHS/ -- T32 AG000212/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2013 Jan 11;339(6116):211-4. doi: 10.1126/science.1227166. Epub 2012 Dec 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23223453" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Hydroxybutyric Acid/blood/*metabolism/pharmacology ; Acetylation ; Animals ; Caloric Restriction ; Catalase/metabolism ; Fasting ; Forkhead Transcription Factors/genetics ; HEK293 Cells ; Histone Deacetylase Inhibitors/blood/*metabolism/pharmacology ; Histone Deacetylases/genetics/*metabolism ; Histones/metabolism ; Humans ; Kidney/drug effects/*metabolism ; Lipid Peroxidation ; Metallothionein/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; *Oxidative Stress/genetics ; Promoter Regions, Genetic ; RNA, Small Interfering ; Superoxide Dismutase/metabolism ; Transcription, Genetic ; Transcriptional Activation
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    Global network reorganization during dynamic adaptations of Bacillus subtilis metabolism (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-03-03
    Description: Adaptation of cells to environmental changes requires dynamic interactions between metabolic and regulatory networks, but studies typically address only one or a few layers of regulation. For nutritional shifts between two preferred carbon sources of Bacillus subtilis, we combined statistical and model-based data analyses of dynamic transcript, protein, and metabolite abundances and promoter activities. Adaptation to malate was rapid and primarily controlled posttranscriptionally compared with the slow, mainly transcriptionally controlled adaptation to glucose that entailed nearly half of the known transcription regulation network. Interactions across multiple levels of regulation were involved in adaptive changes that could also be achieved by controlling single genes. Our analysis suggests that global trade-offs and evolutionary constraints provide incentives to favor complex control programs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buescher, Joerg Martin -- Liebermeister, Wolfram -- Jules, Matthieu -- Uhr, Markus -- Muntel, Jan -- Botella, Eric -- Hessling, Bernd -- Kleijn, Roelco Jacobus -- Le Chat, Ludovic -- Lecointe, Francois -- Mader, Ulrike -- Nicolas, Pierre -- Piersma, Sjouke -- Rugheimer, Frank -- Becher, Dorte -- Bessieres, Philippe -- Bidnenko, Elena -- Denham, Emma L -- Dervyn, Etienne -- Devine, Kevin M -- Doherty, Geoff -- Drulhe, Samuel -- Felicori, Liza -- Fogg, Mark J -- Goelzer, Anne -- Hansen, Annette -- Harwood, Colin R -- Hecker, Michael -- Hubner, Sebastian -- Hultschig, Claus -- Jarmer, Hanne -- Klipp, Edda -- Leduc, Aurelie -- Lewis, Peter -- Molina, Frank -- Noirot, Philippe -- Peres, Sabine -- Pigeonneau, Nathalie -- Pohl, Susanne -- Rasmussen, Simon -- Rinn, Bernd -- Schaffer, Marc -- Schnidder, Julian -- Schwikowski, Benno -- Van Dijl, Jan Maarten -- Veiga, Patrick -- Walsh, Sean -- Wilkinson, Anthony J -- Stelling, Jorg -- Aymerich, Stephane -- Sauer, Uwe -- New York, N.Y. -- Science. 2012 Mar 2;335(6072):1099-103. doi: 10.1126/science.1206871.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Systems Biology, ETH Zurich, Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22383848" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Algorithms ; Bacillus subtilis/*genetics/*metabolism ; Bacterial Proteins/metabolism ; Computer Simulation ; Data Interpretation, Statistical ; Gene Expression Regulation, Bacterial ; *Gene Regulatory Networks ; Genome, Bacterial ; Glucose/*metabolism ; Malates/*metabolism ; Metabolic Networks and Pathways/*genetics ; Metabolome ; Metabolomics ; Models, Biological ; Operon ; Promoter Regions, Genetic ; Transcription Factors/metabolism ; Transcription, Genetic
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    Mitochondrial import efficiency of ATFS-1 regulates mitochondrial UPR activation (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-06-16
    Description: To better understand the response to mitochondrial dysfunction, we examined the mechanism by which ATFS-1 (activating transcription factor associated with stress-1) senses mitochondrial stress and communicates with the nucleus during the mitochondrial unfolded protein response (UPR(mt)) in Caenorhabditis elegans. We found that the key point of regulation is the mitochondrial import efficiency of ATFS-1. In addition to a nuclear localization sequence, ATFS-1 has an N-terminal mitochondrial targeting sequence that is essential for UPR(mt) repression. Normally, ATFS-1 is imported into mitochondria and degraded. However, during mitochondrial stress, we found that import efficiency was reduced, allowing a percentage of ATFS-1 to accumulate in the cytosol and traffic to the nucleus. Our results show that cells monitor mitochondrial import efficiency via ATFS-1 to coordinate the level of mitochondrial dysfunction with the protective transcriptional response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518298/" 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/PMC3518298/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nargund, Amrita M -- Pellegrino, Mark W -- Fiorese, Christopher J -- Baker, Brooke M -- Haynes, Cole M -- R01 AG040061/AG/NIA NIH HHS/ -- R01AG040061/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 3;337(6094):587-90. doi: 10.1126/science.1223560. Epub 2012 Jun 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22700657" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Caenorhabditis elegans/genetics/*metabolism ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Cell Nucleus/*metabolism ; Gene Expression Regulation ; Mitochondria/*metabolism ; Nuclear Localization Signals/genetics/metabolism ; *Stress, Physiological ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic ; *Unfolded Protein Response
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    Tuning of natural killer cell reactivity by NKp46 and Helios calibrates T cell responses (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-01-24
    Description: Natural killer (NK) cells are lymphocytes involved in antimicrobial and antitumoral immune responses. Using N-ethyl-N-nitrosourea mutagenesis in mice, we identified a mutant with increased resistance to viral infections because of the presence of hyperresponsive NK cells. Whole-genome sequencing and functional analysis revealed a loss-of-function mutation in the Ncr1 gene encoding the activating receptor NKp46. The down-regulation of NK cell activity by NKp46 was associated with the silencing of the Helios transcription factor in NK cells. NKp46 was critical for the subsequent development of antiviral and antibacterial T cell responses, which suggests that the regulation of NK cell function by NKp46 allows for the optimal development of adaptive immune responses. NKp46 blockade enhanced NK cell reactivity in vivo, which could enable the design of immunostimulation strategies in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Narni-Mancinelli, Emilie -- Jaeger, Baptiste N -- Bernat, Claire -- Fenis, Aurore -- Kung, Sam -- De Gassart, Aude -- Mahmood, Sajid -- Gut, Marta -- Heath, Simon C -- Estelle, Jordi -- Bertosio, Elodie -- Vely, Frederic -- Gastinel, Louis N -- Beutler, Bruce -- Malissen, Bernard -- Malissen, Marie -- Gut, Ivo G -- Vivier, Eric -- Ugolini, Sophie -- New York, N.Y. -- Science. 2012 Jan 20;335(6066):344-8. doi: 10.1126/science.1215621.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie de Marseille-Luminy, Aix-Marseille University, Campus de Luminy case 906, 13288 Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22267813" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Amino Acid Substitution ; Animals ; Antibodies, Blocking/immunology ; Antibodies, Monoclonal/immunology ; Antigens, Ly/genetics/immunology/*physiology ; CD8-Positive T-Lymphocytes/immunology ; Cell Line ; DNA-Binding Proteins/*genetics/physiology ; Down-Regulation ; Genetic Complementation Test ; Herpesviridae Infections/*immunology/virology ; Immunologic Memory ; Killer Cells, Natural/*immunology ; Listeriosis/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muromegalovirus/physiology ; Mutagenesis ; Natural Cytotoxicity Triggering Receptor 1/antagonists & ; inhibitors/genetics/immunology/*physiology ; T-Lymphocytes/*immunology ; Transcription Factors/*genetics/physiology ; Transcription, Genetic ; Viral Load
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    Organization of the influenza virus replication machinery (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-11-28
    Description: Influenza virus ribonucleoprotein complexes (RNPs) are central to the viral life cycle and in adaptation to new host species. RNPs are composed of the viral genome, viral polymerase, and many copies of the viral nucleoprotein. In vitro cell expression of all RNP protein components with four of the eight influenza virus gene segments enabled structural determination of native influenza virus RNPs by means of cryogenic electron microscopy (cryo-EM). The cryo-EM structure reveals the architecture and organization of the native RNP, defining the attributes of its largely helical structure and how polymerase interacts with nucleoprotein and the viral genome. Observations of branched-RNP structures in negative-stain electron microscopy and their putative identification as replication intermediates suggest a mechanism for viral replication by a second polymerase on the RNP template.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578580/" 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/PMC3578580/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moeller, Arne -- Kirchdoerfer, Robert N -- Potter, Clinton S -- Carragher, Bridget -- Wilson, Ian A -- 2P41RR017573-11/RR/NCRR NIH HHS/ -- 9 P41 GM103310-11/GM/NIGMS NIH HHS/ -- AI058113/AI/NIAID NIH HHS/ -- GM095573/GM/NIGMS NIH HHS/ -- P01 AI058113/AI/NIAID NIH HHS/ -- P41 GM103310/GM/NIGMS NIH HHS/ -- P50GM073197/GM/NIGMS NIH HHS/ -- R01 GM095573/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Dec 21;338(6114):1631-4. doi: 10.1126/science.1227270. Epub 2012 Nov 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Resource for Automated Molecular Microscopy, Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23180774" target="_blank"〉PubMed〈/a〉
    Keywords: Cryoelectron Microscopy ; Crystallography, X-Ray ; Genome, Viral ; Image Processing, Computer-Assisted ; Influenza A Virus, H1N1 Subtype/*chemistry/genetics/physiology/*ultrastructure ; Microscopy, Electron ; Models, Molecular ; Nucleic Acid Conformation ; Protein Conformation ; Protein Subunits/chemistry/metabolism ; RNA Replicase/*chemistry/metabolism/ultrastructure ; RNA, Viral/*chemistry/metabolism/ultrastructure ; RNA-Binding Proteins/chemistry/metabolism/ultrastructure ; Ribonucleoproteins/*chemistry/genetics/metabolism/ultrastructure ; Transcription, Genetic ; Viral Core Proteins/chemistry/metabolism/ultrastructure ; Viral Proteins/*chemistry/metabolism/ultrastructure ; *Virus Replication
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    Transcription-independent function of Polycomb group protein PSC in cell cycle control (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-12
    Description: Polycomb group (PcG) proteins control development and cell proliferation through chromatin-mediated transcriptional repression. We describe a transcription-independent function for PcG protein Posterior sex combs (PSC) in regulating the destruction of cyclin B (CYC-B). A substantial portion of PSC was found outside canonical PcG complexes, instead associated with CYC-B and the anaphase-promoting complex (APC). Cell-based experiments and reconstituted reactions established that PSC and Lemming (LMG, also called APC11) associate and ubiquitylate CYC-B cooperatively, marking it for proteosomal degradation. Thus, PSC appears to mediate both developmental gene silencing and posttranslational control of mitosis. Direct regulation of cell cycle progression might be a crucial part of the PcG system's function in development and cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mohd-Sarip, Adone -- Lagarou, Anna -- Doyen, Cecile M -- van der Knaap, Jan A -- Aslan, Ulku -- Bezstarosti, Karel -- Yassin, Yasmin -- Brock, Hugh W -- Demmers, Jeroen A A -- Verrijzer, C Peter -- New York, N.Y. -- Science. 2012 May 11;336(6082):744-7. doi: 10.1126/science.1215927. Epub 2012 Apr 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Centre for Biomedical Genetics, Erasmus University Medical Centre, Post Office Box 1738, 3000 DR, Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22491092" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase-Promoting Complex-Cyclosome ; Animals ; Apc11 Subunit, Anaphase-Promoting Complex-Cyclosome ; Carrier Proteins/metabolism ; *Cell Cycle Checkpoints ; Cell Line ; Compound Eye, Arthropod/growth & development/metabolism ; Cyclin B/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/cytology/embryology/metabolism ; G2 Phase Cell Cycle Checkpoints ; Gene Silencing ; Imaginal Discs/metabolism ; *Mitosis ; Phenotype ; Polycomb Repressive Complex 1 ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; RNA Interference ; Transcription, Genetic ; Ubiquitin-Protein Ligase Complexes/metabolism ; Ubiquitination ; Wings, Animal/growth & development
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    MORC family ATPases required for heterochromatin condensation and gene silencing (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-05
    Description: Transposable elements (TEs) and DNA repeats are commonly targeted by DNA and histone methylation to achieve epigenetic gene silencing. We isolated mutations in two Arabidopsis genes, AtMORC1 and AtMORC6, which cause derepression of DNA-methylated genes and TEs but no losses of DNA or histone methylation. AtMORC1 and AtMORC6 are members of the conserved Microrchidia (MORC) adenosine triphosphatase (ATPase) family, which are predicted to catalyze alterations in chromosome superstructure. The atmorc1 and atmorc6 mutants show decondensation of pericentromeric heterochromatin, increased interaction of pericentromeric regions with the rest of the genome, and transcriptional defects that are largely restricted to loci residing in pericentromeric regions. Knockdown of the single MORC homolog in Caenorhabditis elegans also impairs transgene silencing. We propose that the MORC ATPases are conserved regulators of gene silencing in eukaryotes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376212/" 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/PMC3376212/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moissiard, Guillaume -- Cokus, Shawn J -- Cary, Joshua -- Feng, Suhua -- Billi, Allison C -- Stroud, Hume -- Husmann, Dylan -- Zhan, Ye -- Lajoie, Bryan R -- McCord, Rachel Patton -- Hale, Christopher J -- Feng, Wei -- Michaels, Scott D -- Frand, Alison R -- Pellegrini, Matteo -- Dekker, Job -- Kim, John K -- Jacobsen, Steven E -- F32 GM100617/GM/NIGMS NIH HHS/ -- F32GM100617/GM/NIGMS NIH HHS/ -- GM007185/GM/NIGMS NIH HHS/ -- GM075060/GM/NIGMS NIH HHS/ -- GM088565/GM/NIGMS NIH HHS/ -- GM60398/GM/NIGMS NIH HHS/ -- HG003143/HG/NHGRI NIH HHS/ -- R01 GM075060/GM/NIGMS NIH HHS/ -- R01 GM088565/GM/NIGMS NIH HHS/ -- R01 HG003143/HG/NHGRI NIH HHS/ -- R37 GM060398/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jun 15;336(6087):1448-51. doi: 10.1126/science.1221472. Epub 2012 May 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cell, and Developmental Biology, University of California at Los Angeles, Terasaki Life Sciences Building, 610 Charles Young Drive East, Los Angeles, CA 90095-723905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22555433" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/chemistry/genetics/*metabolism ; Animals ; Arabidopsis/enzymology/*genetics/*metabolism ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Caenorhabditis elegans ; Caenorhabditis elegans Proteins/genetics/metabolism ; Centromere ; DNA Methylation ; DNA Transposable Elements ; *Gene Silencing ; Genes, Plant ; Heterochromatin/*metabolism/ultrastructure ; Histones/metabolism ; Methylation ; Mutation ; RNA, Small Interfering/metabolism ; Transcription, Genetic ; Transgenes ; Up-Regulation
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    Cold-inducible RNA-binding protein modulates circadian gene expression posttranscriptionally (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-08-28
    Description: In mammalian tissues, circadian gene expression can be driven by local oscillators or systemic signals controlled by the master pacemaker in the suprachiasmatic nucleus. We show that simulated body temperature cycles, but not peripheral oscillators, controlled the rhythmic expression of cold-inducible RNA-binding protein (CIRP) in cultured fibroblasts. In turn, loss-of-function experiments indicated that CIRP was required for high-amplitude circadian gene expression. The transcriptome-wide identification of CIRP-bound RNAs by a biotin-streptavidin-based cross-linking and immunoprecipitation (CLIP) procedure revealed several transcripts encoding circadian oscillator proteins, including CLOCK. Moreover, CLOCK accumulation was strongly reduced in CIRP-depleted fibroblasts. Because ectopic expression of CLOCK improved circadian gene expression in these cells, we surmise that CIRP confers robustness to circadian oscillators through regulation of CLOCK expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morf, Jorg -- Rey, Guillaume -- Schneider, Kim -- Stratmann, Markus -- Fujita, Jun -- Naef, Felix -- Schibler, Ueli -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):379-83. doi: 10.1126/science.1217726. Epub 2012 Aug 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Geneva, and National Centre of Competence in Research, Frontiers in Genetics, 30 Quai Ernest Ansermet, CH-1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22923437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotin ; CLOCK Proteins/*genetics/metabolism ; Chromatin Immunoprecipitation ; Circadian Rhythm/*genetics ; Cold Temperature ; Fibroblasts/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation ; Mice ; NIH 3T3 Cells ; RNA, Messenger/genetics/metabolism ; RNA-Binding Proteins/genetics/*metabolism ; Streptavidin ; Transcription, Genetic
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    Atg7 modulates p53 activity to regulate cell cycle and survival during metabolic stress (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-04-14
    Description: Withdrawal of nutrients triggers an exit from the cell division cycle, the induction of autophagy, and eventually the activation of cell death pathways. The relation, if any, among these events is not well characterized. We found that starved mouse embryonic fibroblasts lacking the essential autophagy gene product Atg7 failed to undergo cell cycle arrest. Independent of its E1-like enzymatic activity, Atg7 could bind to the tumor suppressor p53 to regulate the transcription of the gene encoding the cell cycle inhibitor p21(CDKN1A). With prolonged metabolic stress, the absence of Atg7 resulted in augmented DNA damage with increased p53-dependent apoptosis. Inhibition of the DNA damage response by deletion of the protein kinase Chk2 partially rescued postnatal lethality in Atg7(-/-) mice. Thus, when nutrients are limited, Atg7 regulates p53-dependent cell cycle and cell death pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721513/" 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/PMC4721513/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, In Hye -- Kawai, Yoshichika -- Fergusson, Maria M -- Rovira, Ilsa I -- Bishop, Alexander J R -- Motoyama, Noboru -- Cao, Liu -- Finkel, Toren -- Z01 HL005012-12/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 13;336(6078):225-8. doi: 10.1126/science.1218395.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Medicine, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22499945" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Autophagy ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Line, Tumor ; Cells, Cultured ; Checkpoint Kinase 2 ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; DNA Damage ; Gene Expression Regulation ; Humans ; Mice ; Microtubule-Associated Proteins/genetics/*metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Binding ; Protein Multimerization ; Protein-Serine-Threonine Kinases/genetics ; *Stress, Physiological ; Transcription, Genetic ; Tumor Suppressor Protein p53/*metabolism ; Ubiquitin-Activating Enzymes/genetics/*metabolism
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    Evidence of abundant purifying selection in humans for recently acquired regulatory functions (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-08
    Description: Although only 5% of the human genome is conserved across mammals, a substantially larger portion is biochemically active, raising the question of whether the additional elements evolve neutrally or confer a lineage-specific fitness advantage. To address this question, we integrate human variation information from the 1000 Genomes Project and activity data from the ENCODE Project. A broad range of transcribed and regulatory nonconserved elements show decreased human diversity, suggesting lineage-specific purifying selection. Conversely, conserved elements lacking activity show increased human diversity, suggesting that some recently became nonfunctional. Regulatory elements under human constraint in nonconserved regions were found near color vision and nerve-growth genes, consistent with purifying selection for recently evolved functions. Our results suggest continued turnover in regulatory regions, with at least an additional 4% of the human genome subject to lineage-specific constraint.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104271/" 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/PMC4104271/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ward, Lucas D -- Kellis, Manolis -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01HG004037/HG/NHGRI NIH HHS/ -- RC1 HG005334/HG/NHGRI NIH HHS/ -- RC1HG005334/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1675-8. Epub 2012 Sep 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22956687" target="_blank"〉PubMed〈/a〉
    Keywords: Conserved Sequence ; Disease/genetics ; *Gene Expression Regulation ; *Genetic Variation ; Genome, Human/*genetics ; Humans ; Polymorphism, Single Nucleotide ; Regulatory Sequences, Nucleic Acid/*genetics ; *Selection, Genetic ; Transcription, Genetic
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    FKF1 conveys timing information for CONSTANS stabilization in photoperiodic flowering (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-05-26
    Description: Plants use day-length information to coordinate flowering time with the appropriate season to maximize reproduction. In Arabidopsis, the long day-specific expression of CONSTANS (CO) protein is crucial for flowering induction. Although light signaling regulates CO protein stability, the mechanism by which CO is stabilized in the long-day afternoon has remained elusive. Here, we demonstrate that FLAVIN-BINDING, KELCH REPEAT, F-BOX 1 (FKF1) protein stabilizes CO protein in the afternoon in long days. FKF1 interacts with CO through its LOV domain, and blue light enhances this interaction. In addition, FKF1 simultaneously removes CYCLING DOF FACTOR 1 (CDF1), which represses CO and FLOWERING LOCUS T (FT) transcription. Together with CO transcriptional regulation, FKF1 protein controls robust FT mRNA induction through multiple feedforward mechanisms that accurately control flowering timing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3737243/" 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/PMC3737243/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Young Hun -- Smith, Robert W -- To, Benjamin J -- Millar, Andrew J -- Imaizumi, Takato -- BB/F005237/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F59011/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/G019621/Biotechnology and Biological Sciences Research Council/United Kingdom -- GM079712/GM/NIGMS NIH HHS/ -- R01 GM079712/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 May 25;336(6084):1045-9. doi: 10.1126/science.1219644.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22628657" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/growth & development/metabolism/*physiology ; Arabidopsis Proteins/chemistry/*genetics/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Flowers/*growth & development ; Gene Expression Regulation, Plant ; Light ; Models, Biological ; Mutation ; *Photoperiod ; Plants, Genetically Modified ; Promoter Regions, Genetic ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Stability ; RNA, Messenger/genetics/metabolism ; RNA, Plant/genetics/metabolism ; Repressor Proteins/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
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    Synthetic genetic polymers capable of heredity and evolution (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-04-21
    Description: Genetic information storage and processing rely on just two polymers, DNA and RNA, yet whether their role reflects evolutionary history or fundamental functional constraints is currently unknown. With the use of polymerase evolution and design, we show that genetic information can be stored in and recovered from six alternative genetic polymers based on simple nucleic acid architectures not found in nature [xeno-nucleic acids (XNAs)]. We also select XNA aptamers, which bind their targets with high affinity and specificity, demonstrating that beyond heredity, specific XNAs have the capacity for Darwinian evolution and folding into defined structures. Thus, heredity and evolution, two hallmarks of life, are not limited to DNA and RNA but are likely to be emergent properties of polymers capable of information storage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3362463/" 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/PMC3362463/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pinheiro, Vitor B -- Taylor, Alexander I -- Cozens, Christopher -- Abramov, Mikhail -- Renders, Marleen -- Zhang, Su -- Chaput, John C -- Wengel, Jesper -- Peak-Chew, Sew-Yeu -- McLaughlin, Stephen H -- Herdewijn, Piet -- Holliger, Philipp -- BB/I004793/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- MC_U105178804/Medical Research Council/United Kingdom -- U.1051.03.006(78804)/Medical Research Council/United Kingdom -- U105178804/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Apr 20;336(6079):341-4. doi: 10.1126/science.1217622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council 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/22517858" target="_blank"〉PubMed〈/a〉
    Keywords: Aptamers, Nucleotide/*chemistry/genetics/*metabolism ; DNA/chemistry/genetics ; DNA-Directed DNA Polymerase/chemistry/genetics/metabolism ; Directed Molecular Evolution ; *Evolution, Molecular ; *Molecular Mimicry ; Nucleic Acids/*chemistry/genetics/metabolism ; Polymers/*chemistry/metabolism ; RNA/chemistry/genetics ; RNA-Directed DNA Polymerase/chemistry/metabolism ; Reverse Transcription ; Templates, Genetic ; Transcription, Genetic
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    Developmental pattern formation: insights from physics and biology (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-10-16
    Description: The spatial organization of cell fates during development involves the interpretation of morphogen gradients by cellular signaling cascades and transcriptional networks. Recent studies use biophysical models, genetics, and quantitative imaging to unravel how tissue-level morphogen behavior arises from subcellular events. Moreover, data from several systems show that morphogen gradients, downstream signaling, and the activity of cell-intrinsic transcriptional networks change dynamically during pattern formation. Studies from Drosophila and now also vertebrates suggest that transcriptional network dynamics are central to the generation of gene expression patterns. Together, this leads to the view that pattern formation is an emergent behavior that results from the coordination of events occurring across molecular, cellular, and tissue scales. The development of novel approaches to study this complex process remains a challenge.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kicheva, Anna -- Cohen, Michael -- Briscoe, James -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Oct 12;338(6104):210-2. doi: 10.1126/science.1225182.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council-National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23066071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning/*genetics ; Drosophila/embryology/genetics ; *Gene Expression Regulation, Developmental ; Gene Regulatory Networks ; Transcription, Genetic
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    Egg cell-secreted EC1 triggers sperm cell activation during double fertilization (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-11-28
    Description: Double fertilization is the defining characteristic of flowering plants. However, the molecular mechanisms regulating the fusion of one sperm with the egg and the second sperm with the central cell are largely unknown. We show that gamete interactions in Arabidopsis depend on small cysteine-rich EC1 (EGG CELL 1) proteins accumulating in storage vesicles of the egg cell. Upon sperm arrival, EC1-containing vesicles are exocytosed. The sperm endomembrane system responds to exogenously applied EC1 peptides by redistributing the potential gamete fusogen HAP2/GCS1 (HAPLESS 2/GENERATIVE CELL SPECIFIC 1) to the cell surface. Furthermore, fertilization studies with ec1 quintuple mutants show that successful male-female gamete interactions are necessary to prevent multiple-sperm cell delivery. Our findings provide evidence that mutual gamete activation, regulated exocytosis, and sperm plasma membrane modifications govern flowering plant gamete interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sprunck, Stefanie -- Rademacher, Svenja -- Vogler, Frank -- Gheyselinck, Jacqueline -- Grossniklaus, Ueli -- Dresselhaus, Thomas -- New York, N.Y. -- Science. 2012 Nov 23;338(6110):1093-7. doi: 10.1126/science.1223944.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Plant Biochemistry, Biochemie-Zentrum Regensburg, University of Regensburg, Universitatsstrasse 31, D-93053 Regensburg, Germany. stefanie.sprunck@biologie.uni-regensburg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23180860" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/genetics/metabolism/*physiology ; Arabidopsis Proteins/genetics/*metabolism ; Carrier Proteins/metabolism ; Cell Membrane/metabolism ; *Exocytosis ; *Fertilization ; Flowers/genetics/metabolism/physiology ; Gene Expression Regulation, Plant ; Genes, Plant ; Molecular Sequence Data ; Multigene Family ; Ovule/genetics/metabolism/physiology ; Pollen/genetics/metabolism/*physiology ; Protein Sorting Signals ; Transcription, Genetic
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    AID-driven deletion causes immunoglobulin heavy chain locus suicide recombination in B cells (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-04-28
    Description: Remodeling of immunoglobulin genes by activation-induced deaminase (AID) is required for affinity maturation and class-switch recombination in mature B lymphocytes. In the immunoglobulin heavy chain locus, these processes are predominantly controlled by the 3' cis-regulatory region. We now show that this region is transcribed and undergoes AID-mediated mutation and recombination around phylogenetically conserved switchlike DNA repeats. Such recombination, which we term locus suicide recombination, deletes the whole constant region gene cluster and thus stops expression of the immunoglobulin of the B cell surface, which is critical for B cell survival. The frequency of this event is approaching that of class switching and makes it a potential regulator of B cell homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peron, Sophie -- Laffleur, Brice -- Denis-Lagache, Nicolas -- Cook-Moreau, Jeanne -- Tinguely, Aurelien -- Delpy, Laurent -- Denizot, Yves -- Pinaud, Eric -- Cogne, Michel -- New York, N.Y. -- Science. 2012 May 18;336(6083):931-4. doi: 10.1126/science.1218692. Epub 2012 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Limoges University, CNRS, 2 rue Marcland, 87025 Limoges Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22539552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/*physiology ; Base Sequence ; Cell Line ; Cell Survival ; Cytidine Deaminase/*metabolism ; *Gene Deletion ; *Gene Rearrangement, B-Lymphocyte, Heavy Chain ; *Genes, Immunoglobulin Heavy Chain ; Homeostasis ; Humans ; Immunoglobulin Class Switching ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; *Recombination, Genetic ; Regulatory Sequences, Nucleic Acid ; Repetitive Sequences, Nucleic Acid ; Transcription, Genetic
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    Experimental evidence supports a sex-specific selective sieve in mitochondrial genome evolution (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-14
    Description: Mitochondria are maternally transmitted; hence, their genome can only make a direct and adaptive response to selection through females, whereas males represent an evolutionary dead end. In theory, this creates a sex-specific selective sieve, enabling deleterious mutations to accumulate in mitochondrial genomes if they exert male-specific effects. We tested this hypothesis, expressing five mitochondrial variants alongside a standard nuclear genome in Drosophila melanogaster, and found striking sexual asymmetry in patterns of nuclear gene expression. Mitochondrial polymorphism had few effects on nuclear gene expression in females but major effects in males, modifying nearly 10% of transcripts. These were mostly male-biased in expression, with enrichment hotspots in the testes and accessory glands. Our results suggest an evolutionary mechanism that results in mitochondrial genomes harboring male-specific mutation loads.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Innocenti, Paolo -- Morrow, Edward H -- Dowling, Damian K -- New York, N.Y. -- Science. 2011 May 13;332(6031):845-8. doi: 10.1126/science.1201157.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Genetics, Evolutionary Biology Centre, Uppsala University, Norbyvagen 18-D, 75236 Uppsala, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21566193" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/genetics ; DNA, Mitochondrial/genetics ; Drosophila melanogaster/*genetics/physiology ; *Evolution, Molecular ; Female ; Fertility ; *Gene Expression ; Gene Expression Profiling ; Genes, Insect ; Genetic Fitness ; *Genome, Insect ; *Genome, Mitochondrial ; Male ; *Mutation ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Genetic ; Selection, Genetic ; Sex Characteristics ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Aberrant overexpression of satellite repeats in pancreatic and other epithelial cancers (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-15
    Description: Satellite repeats in heterochromatin are transcribed into noncoding RNAs that have been linked to gene silencing and maintenance of chromosomal integrity. Using digital gene expression analysis, we showed that these transcripts are greatly overexpressed in mouse and human epithelial cancers. In 8 of 10 mouse pancreatic ductal adenocarcinomas (PDACs), pericentromeric satellites accounted for a mean 12% (range 1 to 50%) of all cellular transcripts, a mean 40-fold increase over that in normal tissue. In 15 of 15 human PDACs, alpha satellite transcripts were most abundant and HSATII transcripts were highly specific for cancer. Similar patterns were observed in cancers of the lung, kidney, ovary, colon, and prostate. Derepression of satellite transcripts correlated with overexpression of the long interspersed nuclear element 1 (LINE-1) retrotransposon and with aberrant expression of neuroendocrine-associated genes proximal to LINE-1 insertions. The overexpression of satellite transcripts in cancer may reflect global alterations in heterochromatin silencing and could potentially be useful as a biomarker for cancer detection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701432/" 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/PMC3701432/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ting, David T -- Lipson, Doron -- Paul, Suchismita -- Brannigan, Brian W -- Akhavanfard, Sara -- Coffman, Erik J -- Contino, Gianmarco -- Deshpande, Vikram -- Iafrate, A John -- Letovsky, Stan -- Rivera, Miguel N -- Bardeesy, Nabeel -- Maheswaran, Shyamala -- Haber, Daniel A -- CA129933/CA/NCI NIH HHS/ -- L30 CA142210/CA/NCI NIH HHS/ -- P01 CA117969/CA/NCI NIH HHS/ -- R01 CA129933/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Feb 4;331(6017):593-6. doi: 10.1126/science.1200801. Epub 2011 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21233348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma in Situ/genetics/pathology ; Carcinoma, Pancreatic Ductal/genetics/pathology ; Colonic Neoplasms/genetics/pathology ; DNA Methylation ; DNA, Neoplasm/genetics ; DNA, Satellite/*genetics ; Female ; Gene Expression ; Gene Expression Profiling ; Heterochromatin/chemistry/genetics ; Humans ; Long Interspersed Nucleotide Elements ; Lung Neoplasms/genetics/pathology ; Male ; Mice ; Mice, Nude ; Neoplasms/*genetics/pathology ; Neurosecretory Systems/metabolism ; Ovarian Neoplasms/genetics/pathology ; Pancreatic Neoplasms/*genetics/pathology ; Prostatic Neoplasms/genetics/pathology ; RNA, Neoplasm/*genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Comparative functional genomics of the fission yeasts (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-23
    Description: The fission yeast clade--comprising Schizosaccharomyces pombe, S. octosporus, S. cryophilus, and S. japonicus--occupies the basal branch of Ascomycete fungi and is an important model of eukaryote biology. A comparative annotation of these genomes identified a near extinction of transposons and the associated innovation of transposon-free centromeres. Expression analysis established that meiotic genes are subject to antisense transcription during vegetative growth, which suggests a mechanism for their tight regulation. In addition, trans-acting regulators control new genes within the context of expanded functional modules for meiosis and stress response. Differences in gene content and regulation also explain why, unlike the budding yeast of Saccharomycotina, fission yeasts cannot use ethanol as a primary carbon source. These analyses elucidate the genome structure and gene regulation of fission yeast and provide tools for investigation across the Schizosaccharomyces clade.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131103/" 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/PMC3131103/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhind, Nicholas -- Chen, Zehua -- Yassour, Moran -- Thompson, Dawn A -- Haas, Brian J -- Habib, Naomi -- Wapinski, Ilan -- Roy, Sushmita -- Lin, Michael F -- Heiman, David I -- Young, Sarah K -- Furuya, Kanji -- Guo, Yabin -- Pidoux, Alison -- Chen, Huei Mei -- Robbertse, Barbara -- Goldberg, Jonathan M -- Aoki, Keita -- Bayne, Elizabeth H -- Berlin, Aaron M -- Desjardins, Christopher A -- Dobbs, Edward -- Dukaj, Livio -- Fan, Lin -- FitzGerald, Michael G -- French, Courtney -- Gujja, Sharvari -- Hansen, Klavs -- Keifenheim, Dan -- Levin, Joshua Z -- Mosher, Rebecca A -- Muller, Carolin A -- Pfiffner, Jenna -- Priest, Margaret -- Russ, Carsten -- Smialowska, Agata -- Swoboda, Peter -- Sykes, Sean M -- Vaughn, Matthew -- Vengrova, Sonya -- Yoder, Ryan -- Zeng, Qiandong -- Allshire, Robin -- Baulcombe, David -- Birren, Bruce W -- Brown, William -- Ekwall, Karl -- Kellis, Manolis -- Leatherwood, Janet -- Levin, Henry -- Margalit, Hanah -- Martienssen, Rob -- Nieduszynski, Conrad A -- Spatafora, Joseph W -- Friedman, Nir -- Dalgaard, Jacob Z -- Baumann, Peter -- Niki, Hironori -- Regev, Aviv -- Nusbaum, Chad -- BB/E023754/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- DP1 OD003958/OD/NIH HHS/ -- R01 GM069957/GM/NIGMS NIH HHS/ -- R01 GM076396/GM/NIGMS NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-06/HG/NHGRI NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 May 20;332(6032):930-6. doi: 10.1126/science.1203357. Epub 2011 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA. nick.rhind@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21511999" target="_blank"〉PubMed〈/a〉
    Keywords: Centromere/genetics/physiology/ultrastructure ; DNA Transposable Elements ; Evolution, Molecular ; Gene Expression Profiling ; Gene Expression Regulation, Fungal ; Genes, Mating Type, Fungal ; *Genome, Fungal ; Genomics ; Glucose/metabolism ; Meiosis ; Molecular Sequence Annotation ; Molecular Sequence Data ; Phylogeny ; RNA, Antisense/genetics ; RNA, Fungal/genetics ; RNA, Small Interfering/genetics ; RNA, Untranslated/genetics ; Regulatory Elements, Transcriptional ; Schizosaccharomyces/*genetics/growth & development/metabolism ; Schizosaccharomyces pombe Proteins/genetics/metabolism ; Sequence Analysis, DNA ; Species Specificity ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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    The dynamic architecture of Hox gene clusters (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-15
    Description: The spatial and temporal control of Hox gene transcription is essential for patterning the vertebrate body axis. Although this process involves changes in histone posttranslational modifications, the existence of particular three-dimensional (3D) architectures remained to be assessed in vivo. Using high-resolution chromatin conformation capture methodology, we examined the spatial configuration of Hox clusters in embryonic mouse tissues where different Hox genes are active. When the cluster is transcriptionally inactive, Hox genes associate into a single 3D structure delimited from flanking regions. Once transcription starts, Hox clusters switch to a bimodal 3D organization where newly activated genes progressively cluster into a transcriptionally active compartment. This transition in spatial configurations coincides with the dynamics of chromatin marks, which label the progression of the gene clusters from a negative to a positive transcription status. This spatial compartmentalization may be key to process the colinear activation of these compact gene clusters.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noordermeer, Daan -- Leleu, Marion -- Splinter, Erik -- Rougemont, Jacques -- De Laat, Wouter -- Duboule, Denis -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):222-5. doi: 10.1126/science.1207194.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Research Centre Frontiers in Genetics, School of Life Sciences, Ecole Polytechnique Federale (EPFL), Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998387" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/metabolism/ultrastructure ; Embryo, Mammalian/cytology/*metabolism ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Histones/metabolism ; Mice ; Models, Genetic ; *Multigene Family ; Transcription, Genetic ; *Transcriptional Activation
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    Stochastic pulse regulation in bacterial stress response (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-08
    Description: Gene regulatory circuits can use dynamic, and even stochastic, strategies to respond to environmental conditions. We examined activation of the general stress response mediated by the alternative sigma factor, sigma(B), in individual Bacillus subtilis cells. We observed that energy stress activates sigma(B) in discrete stochastic pulses, with increasing levels of stress leading to higher pulse frequencies. By perturbing and rewiring the endogenous system, we found that this behavior results from three key features of the sigma(B) circuit: an ultrasensitive phosphorylation switch; stochasticity ("noise"), which activates that switch; and a mixed (positive and negative) transcriptional feedback, which can both amplify a pulse and switch it off. Together, these results show how prokaryotes encode signals using stochastic pulse frequency modulation through a compact regulatory architecture.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4100694/" 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/PMC4100694/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Locke, James C W -- Young, Jonathan W -- Fontes, Michelle -- Hernandez Jimenez, Maria Jesus -- Elowitz, Michael B -- P50 GM068763/GM/NIGMS NIH HHS/ -- R01 GM079771/GM/NIGMS NIH HHS/ -- R01GM079771/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Oct 21;334(6054):366-9. doi: 10.1126/science.1208144. Epub 2011 Oct 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Division of Biology and Bioengineering, Broad Center, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979936" target="_blank"〉PubMed〈/a〉
    Keywords: Bacillus subtilis/*genetics/metabolism/*physiology ; Bacterial Proteins/genetics/*metabolism ; Carrier Proteins/genetics/metabolism ; Feedback, Physiological ; Gene Expression Regulation, Bacterial ; *Gene Regulatory Networks ; Mycophenolic Acid/pharmacology ; Phosphoric Monoester Hydrolases/genetics/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Sigma Factor/genetics/*metabolism ; Stochastic Processes ; *Stress, Physiological ; Transcription, Genetic
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    Plant science. When vernalization makes sense (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turck, Franziska -- Coupland, George -- New York, N.Y. -- Science. 2011 Jan 7;331(6013):36-7. doi: 10.1126/science.1200786.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Plant Breeding Research, Carl von Linn Weg 10, Cologne, 50829 Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21212342" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*genetics/growth & development/*physiology ; Arabidopsis Proteins/*genetics/metabolism ; *Cold Temperature ; DNA-Binding Proteins/genetics/metabolism ; Flowers/*growth & development ; Gene Expression Regulation, Plant ; Genes, Plant ; MADS Domain Proteins/*genetics/metabolism ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; RNA, Antisense/*genetics/metabolism ; RNA, Messenger/genetics/metabolism ; RNA, Plant/genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; Repressor Proteins/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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    Cell biology. Telling time without turning on genes (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):391. doi: 10.1126/science.331.6016.391.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21273463" target="_blank"〉PubMed〈/a〉
    Keywords: Chlorophyta/metabolism/*physiology ; Circadian Clocks/*physiology ; *Circadian Rhythm ; Erythrocytes/metabolism/*physiology ; Humans ; Oxidation-Reduction ; Peroxiredoxins/*metabolism ; Temperature ; Transcription, Genetic
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    Role for piRNAs and noncoding RNA in de novo DNA methylation of the imprinted mouse Rasgrf1 locus (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-14
    Description: Genomic imprinting causes parental origin-specific monoallelic gene expression through differential DNA methylation established in the parental germ line. However, the mechanisms underlying how specific sequences are selectively methylated are not fully understood. We have found that the components of the PIWI-interacting RNA (piRNA) pathway are required for de novo methylation of the differentially methylated region (DMR) of the imprinted mouse Rasgrf1 locus, but not other paternally imprinted loci. A retrotransposon sequence within a noncoding RNA spanning the DMR was targeted by piRNAs generated from a different locus. A direct repeat in the DMR, which is required for the methylation and imprinting of Rasgrf1, served as a promoter for this RNA. We propose a model in which piRNAs and a target RNA direct the sequence-specific methylation of Rasgrf1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368507/" 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/PMC3368507/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watanabe, Toshiaki -- Tomizawa, Shin-ichi -- Mitsuya, Kohzoh -- Totoki, Yasushi -- Yamamoto, Yasuhiro -- Kuramochi-Miyagawa, Satomi -- Iida, Naoko -- Hoki, Yuko -- Murphy, Patrick J -- Toyoda, Atsushi -- Gotoh, Kengo -- Hiura, Hitoshi -- Arima, Takahiro -- Fujiyama, Asao -- Sado, Takashi -- Shibata, Tatsuhiro -- Nakano, Toru -- Lin, Haifan -- Ichiyanagi, Kenji -- Soloway, Paul D -- Sasaki, Hiroyuki -- R01 CA098597/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 May 13;332(6031):848-52. doi: 10.1126/science.1203919.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Genetics and Department of Integrated Genetics, National Institute of Genetics, Research Organization of Information and Systems, Mishima, Shizuoka, 411-8540, Japan. toshwatatoshiakiwatanabe@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21566194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; *DNA Methylation ; *Genomic Imprinting ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondrial Proteins/genetics/metabolism ; Models, Genetic ; Mutation ; Phospholipase D/genetics/metabolism ; Proteins/genetics/metabolism ; RNA, Small Interfering/*genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; Repetitive Sequences, Nucleic Acid ; Retroelements ; Spermatogonia/metabolism ; Testis/embryology/metabolism ; Transcription, Genetic ; ras-GRF1/*genetics
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    Global DNA demethylation during mouse erythropoiesis in vivo (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-11-15
    Description: In the mammalian genome, 5'-CpG-3' dinucleotides are frequently methylated, correlating with transcriptional silencing. Genome-wide demethylation is thought to occur only twice during development, in primordial germ cells and in the pre-implantation embryo. These demethylation events are followed by de novo methylation, setting up a pattern inherited throughout development and modified only at tissue-specific loci. We studied DNA methylation in differentiating mouse erythroblasts in vivo by using genomic-scale reduced representation bisulfite sequencing (RRBS). Demethylation at the erythroid-specific beta-globin locus was coincident with global DNA demethylation at most genomic elements. Global demethylation was continuous throughout differentiation and required rapid DNA replication. Hence, DNA demethylation can occur globally during somatic cell differentiation, providing an experimental model for its study in development and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230325/" 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/PMC3230325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shearstone, Jeffrey R -- Pop, Ramona -- Bock, Christoph -- Boyle, Patrick -- Meissner, Alexander -- Socolovsky, Merav -- DK32520/DK/NIDDK NIH HHS/ -- R01 HL084168/HL/NHLBI NIH HHS/ -- R01 HL084168-02/HL/NHLBI NIH HHS/ -- R01 HL084168-03/HL/NHLBI NIH HHS/ -- R01 HL084168-04/HL/NHLBI NIH HHS/ -- R01 HL084168-04S1/HL/NHLBI NIH HHS/ -- R01 HL084168-05/HL/NHLBI NIH HHS/ -- T32-130807/PHS HHS/ -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):799-802. doi: 10.1126/science.1207306.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22076376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CpG Islands ; *DNA Methylation ; DNA Replication ; Dinucleoside Phosphates/metabolism ; Embryo, Mammalian ; Erythroblasts/*metabolism ; *Erythropoiesis ; Gene Expression Regulation, Developmental ; Genome ; Liver/embryology ; Locus Control Region ; Long Interspersed Nucleotide Elements ; Mice ; S Phase ; Sequence Analysis, DNA ; Transcription, Genetic ; beta-Globins/genetics
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    Microbiology. A tail of division (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cowman, Alan F -- Tonkin, Christopher J -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):409-10. doi: 10.1126/science.1201692.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3052, Australia. cowman@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21273475" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Protozoan/*metabolism ; Cell Division ; Cell Membrane/metabolism ; Membrane Proteins/metabolism ; Phosphorylation ; Protozoan Proteins/*metabolism ; Signal Transduction ; Toxoplasma/cytology/growth & development/*physiology ; Transcription, Genetic
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    Mutagenic processing of ribonucleotides in DNA by yeast topoisomerase I (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-28
    Description: The ribonuclease (RNase) H class of enzymes degrades the RNA component of RNA:DNA hybrids and is important in nucleic acid metabolism. RNase H2 is specialized to remove single ribonucleotides [ribonucleoside monophosphates (rNMPs)] from duplex DNA, and its absence in budding yeast has been associated with the accumulation of deletions within short tandem repeats. Here, we demonstrate that rNMP-associated deletion formation requires the activity of Top1, a topoisomerase that relaxes supercoils by reversibly nicking duplex DNA. The reported studies extend the role of Top1 to include the processing of rNMPs in genomic DNA into irreversible single-strand breaks, an activity that can have distinct mutagenic consequences and may be relevant to human disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3380281/" 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/PMC3380281/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Nayun -- Huang, Shar-yin N -- Williams, Jessica S -- Li, Yue C -- Clark, Alan B -- Cho, Jang-Eun -- Kunkel, Thomas A -- Pommier, Yves -- Jinks-Robertson, Sue -- R01 GM038464/GM/NIGMS NIH HHS/ -- R01 GM093197/GM/NIGMS NIH HHS/ -- R01 GM38464/GM/NIGMS NIH HHS/ -- R01 GM93197/GM/NIGMS NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Jun 24;332(6037):1561-4. doi: 10.1126/science.1205016.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21700875" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Transport Systems, Basic/genetics ; Base Sequence ; Camptothecin/pharmacology ; Canavanine/pharmacology ; DNA Breaks ; DNA Topoisomerases, Type I/*metabolism ; DNA, Fungal/chemistry/*metabolism ; DNA, Single-Stranded/metabolism ; Microsatellite Repeats ; Molecular Sequence Data ; *Mutagenesis ; Nucleic Acid Conformation ; Ribonuclease H/genetics/metabolism ; Ribonucleotides/*metabolism ; Saccharomyces cerevisiae/enzymology/*genetics/*metabolism ; Saccharomyces cerevisiae Proteins/genetics ; *Sequence Deletion ; Transcription, Genetic
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    Arabidopsis EDS1 connects pathogen effector recognition to cell compartment-specific immune responses (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-12-14
    Description: Pathogen effectors are intercepted by plant intracellular nucleotide binding-leucine-rich repeat (NB-LRR) receptors. However, processes linking receptor activation to downstream defenses remain obscure. Nucleo-cytoplasmic basal resistance regulator EDS1 (ENHANCED DISEASE SUSCEPTIBILITY1) is indispensible for immunity mediated by TIR (Toll-interleukin-1 receptor)-NB-LRR receptors. We show that Arabidopsis EDS1 molecularly connects TIR-NB-LRR disease resistance protein RPS4 recognition of bacterial effector AvrRps4 to defense pathways. RPS4-EDS1 and AvrRps4-EDS1 complexes are detected inside nuclei of living tobacco cells after transient coexpression and in Arabidopsis soluble leaf extracts after resistance activation. Forced AvrRps4 localization to the host cytoplasm or nucleus reveals cell compartment-specific RPS4-EDS1 defense branches. Although nuclear processes restrict bacterial growth, programmed cell death and transcriptional resistance reinforcement require nucleo-cytoplasmic coordination. Thus, EDS1 behaves as an effector target and activated TIR-NB-LRR signal transducer for defenses across cell compartments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heidrich, Katharina -- Wirthmueller, Lennart -- Tasset, Celine -- Pouzet, Cecile -- Deslandes, Laurent -- Parker, Jane E -- New York, N.Y. -- Science. 2011 Dec 9;334(6061):1401-4. doi: 10.1126/science.1211641.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck Institute for Plant Breeding Research, Department of Plant-Microbe Interactions, D-50829 Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22158818" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; Arabidopsis/genetics/*immunology/*metabolism/microbiology ; Arabidopsis Proteins/*metabolism ; Bacterial Proteins/*metabolism ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; DNA-Binding Proteins/*metabolism ; *Immunity, Innate ; Plant Diseases/*immunology/microbiology ; Plant Leaves/microbiology ; Plant Proteins/*metabolism ; Plants, Genetically Modified ; Pseudomonas syringae/growth & development/*immunology ; Recombinant Fusion Proteins/metabolism ; Tobacco ; Transcription, Genetic
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    Molecular biology. Climbing in 190 dimensions (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-04-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yarus, Michael -- New York, N.Y. -- Science. 2011 Apr 8;332(6026):181-2. doi: 10.1126/science.1205379.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, CO 80309, USA. michael.yarus@colorado.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21474742" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Directed Molecular Evolution ; Nucleic Acid Conformation ; Protein Biosynthesis ; RNA/*chemistry/metabolism ; RNA Replicase/*chemistry/*metabolism ; RNA, Catalytic/*chemistry/*metabolism ; Transcription, Genetic
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    Yeast Rrn7 and human TAF1B are TFIIB-related RNA polymerase I general transcription factors (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-17
    Description: Eukaryotic and archaeal multisubunit RNA polymerases (Pols) are structurally related and require several similar components for transcription initiation. However, none of the Pol I factors were known to share homology with transcription factor IIB (TFIIB) or TFIIB-related proteins, key factors in the initiation mechanisms of the other Pols. Here we show that Rrn7, a subunit of the yeast Pol I core factor, and its human ortholog TAF1B are TFIIB-like factors. Although distantly related, Rrn7 shares many activities associated with TFIIB-like factors. Domain swaps between TFIIB-related factors show that Rrn7 is most closely related to the Pol III general factor Brf1. Our results point to the conservation of initiation mechanisms among multisubunit Pols and reveal a key function of yeast core factor/human SL1 in Pol I transcription.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319074/" 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/PMC3319074/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knutson, Bruce A -- Hahn, Steven -- GM053451/GM/NIGMS NIH HHS/ -- R01 GM053451/GM/NIGMS NIH HHS/ -- R01 GM053451-17/GM/NIGMS NIH HHS/ -- T32 CA009657/CA/NCI NIH HHS/ -- T32 CA009657-22/CA/NCI NIH HHS/ -- T32 CA09657/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 Sep 16;333(6049):1637-40. doi: 10.1126/science.1207699.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Division of Basic Sciences, 1100 Fairview Avenue N, Post Office Box 19024, Mailstop A1-162, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921198" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Humans ; Molecular Sequence Data ; Pol1 Transcription Initiation Complex Proteins/*chemistry/genetics/*metabolism ; Protein Folding ; Protein Interaction Domains and Motifs ; Protein Structure, Secondary ; Protein Structure, Tertiary ; RNA Polymerase I/*metabolism ; Saccharomyces cerevisiae Proteins/*chemistry/genetics/*metabolism ; Sequence Alignment ; TATA-Box Binding Protein/metabolism ; Transcription Factor TFIIB/chemistry/metabolism ; Transcription Factor TFIIIB/chemistry/genetics/metabolism ; Transcription, Genetic
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    A molecular mechanism for circadian clock negative feedback (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-06-18
    Description: Circadian rhythms in mammals are generated by a feedback loop in which the three PERIOD (PER) proteins, acting in a large complex, inhibit the transcriptional activity of the CLOCK-BMAL1 dimer, which represses their own expression. Although fundamental, the mechanism of negative feedback in the mammalian clock, or any eukaryotic clock, is unknown. We analyzed protein constituents of PER complexes purified from mouse tissues and identified PSF (polypyrimidine tract-binding protein-associated splicing factor). Our analysis indicates that PSF within the PER complex recruits SIN3A, a scaffold for assembly of transcriptional inhibitory complexes and that the PER complex thereby rhythmically delivers histone deacetylases to the Per1 promoter, which repress Per1 transcription. These findings provide a function for the PER complex and a molecular mechanism for circadian clock negative feedback.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3859310/" 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/PMC3859310/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duong, Hao A -- Robles, Maria S -- Knutti, Darko -- Weitz, Charles J -- T32 NS007484/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2011 Jun 17;332(6036):1436-9. doi: 10.1126/science.1196766.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21680841" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/genetics/metabolism ; Animals ; CLOCK Proteins/genetics/metabolism ; *Circadian Clocks ; *Circadian Rhythm ; Cryptochromes/metabolism ; *Feedback, Physiological ; Histone Deacetylase 1/metabolism ; Histones/metabolism ; Liver/metabolism ; Lung/metabolism ; Mass Spectrometry ; Mice ; Period Circadian Proteins/*genetics/metabolism ; Promoter Regions, Genetic ; RNA-Binding Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/*metabolism ; Transcription, Genetic
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    Molecular biology. A new twist for topoisomerase (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-06-28
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171735/" 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/PMC3171735/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cerritelli, Susana M -- Chon, Hyongi -- Crouch, Robert J -- Z99 HD999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Jun 24;332(6037):1510-1. doi: 10.1126/science.1208450.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Genomics of Development, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21700860" target="_blank"〉PubMed〈/a〉
    Keywords: Autoimmune Diseases of the Nervous System/genetics ; DNA Replication ; DNA Topoisomerases, Type I/*metabolism ; DNA, Fungal/chemistry/genetics/*metabolism ; Humans ; Microsatellite Repeats ; Nervous System Malformations/genetics ; Nucleic Acid Conformation ; Ribonuclease H/genetics/metabolism ; Ribonucleotides/*metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; *Sequence Deletion ; Transcription, Genetic
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    Posttranslational modification of pili upon cell contact triggers N. meningitidis dissemination (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-02-12
    Description: The Gram-negative bacterium Neisseria meningitidis asymptomatically colonizes the throat of 10 to 30% of the human population, but throat colonization can also act as the port of entry to the blood (septicemia) and then the brain (meningitis). Colonization is mediated by filamentous organelles referred to as type IV pili, which allow the formation of bacterial aggregates associated with host cells. We found that proliferation of N. meningitidis in contact with host cells increased the transcription of a bacterial gene encoding a transferase that adds phosphoglycerol onto type IV pili. This unusual posttranslational modification specifically released type IV pili-dependent contacts between bacteria. In turn, this regulated detachment process allowed propagation of the bacterium to new colonization sites and also migration across the epithelium, a prerequisite for dissemination and invasive disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chamot-Rooke, Julia -- Mikaty, Guillain -- Malosse, Christian -- Soyer, Magali -- Dumont, Audrey -- Gault, Joseph -- Imhaus, Anne-Flore -- Martin, Patricia -- Trellet, Mikael -- Clary, Guilhem -- Chafey, Philippe -- Camoin, Luc -- Nilges, Michael -- Nassif, Xavier -- Dumenil, Guillaume -- New York, N.Y. -- Science. 2011 Feb 11;331(6018):778-82. doi: 10.1126/science.1200729.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ecole Polytechnique, Laboratoire des Mecanismes Reactionnels, Palaiseau F-91128, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21311024" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Adhesion ; Cell Line, Tumor ; Epithelial Cells/microbiology ; Fimbriae Proteins/chemistry/*metabolism ; Fimbriae, Bacterial/chemistry/*metabolism ; Gene Expression Regulation, Bacterial ; Glycerol/metabolism ; Humans ; Models, Molecular ; Neisseria meningitidis/genetics/growth & development/*pathogenicity ; Phosphorylation ; Phosphotransferases/*genetics/*metabolism ; *Protein Processing, Post-Translational ; Transcription, Genetic
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    A packing mechanism for nucleosome organization reconstituted across a eukaryotic genome (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-05-21
    Description: Near the 5' end of most eukaryotic genes, nucleosomes form highly regular arrays that begin at canonical distances from the transcriptional start site. Determinants of this and other aspects of genomic nucleosome organization have been ascribed to statistical positioning, intrinsically DNA-encoded positioning, or some aspect of transcription initiation. Here, we provide evidence for a different explanation. Biochemical reconstitution of proper nucleosome positioning, spacing, and occupancy levels was achieved across the 5' ends of most yeast genes by adenosine triphosphate-dependent trans-acting factors. These transcription-independent activities override DNA-intrinsic positioning and maintain uniform spacing at the 5' ends of genes even at low nucleosome densities. Thus, an active, nonstatistical nucleosome packing mechanism creates chromatin organizing centers at the 5' ends of genes where important regulatory elements reside.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Zhenhai -- Wippo, Christian J -- Wal, Megha -- Ward, Elissa -- Korber, Philipp -- Pugh, B Franklin -- HG004160/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2011 May 20;332(6032):977-80. doi: 10.1126/science.1200508.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Eukaryotic Gene Regulation, Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, PA 16802, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21596991" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Base Sequence ; Chromatin Assembly and Disassembly ; Computational Biology ; DNA, Fungal/chemistry/genetics ; *Genes, Fungal ; *Genome, Fungal ; Histones/metabolism ; Nucleosomes/*genetics/*metabolism ; Poly dA-dT/analysis ; Saccharomyces cerevisiae/genetics ; Trans-Activators/genetics/metabolism ; Transcription Initiation Site ; Transcription, Genetic
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    optix drives the repeated convergent evolution of butterfly wing pattern mimicry (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-07-23
    Description: Mimicry--whereby warning signals in different species evolve to look similar--has long served as a paradigm of convergent evolution. Little is known, however, about the genes that underlie the evolution of mimetic phenotypes or to what extent the same or different genes drive such convergence. Here, we characterize one of the major genes responsible for mimetic wing pattern evolution in Heliconius butterflies. Mapping, gene expression, and population genetic work all identify a single gene, optix, that controls extreme red wing pattern variation across multiple species of Heliconius. Our results show that the cis-regulatory evolution of a single transcription factor can repeatedly drive the convergent evolution of complex color patterns in distantly related species, thus blurring the distinction between convergence and homology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reed, Robert D -- Papa, Riccardo -- Martin, Arnaud -- Hines, Heather M -- Counterman, Brian A -- Pardo-Diaz, Carolina -- Jiggins, Chris D -- Chamberlain, Nicola L -- Kronforst, Marcus R -- Chen, Rui -- Halder, Georg -- Nijhout, H Frederik -- McMillan, W Owen -- New York, N.Y. -- Science. 2011 Aug 26;333(6046):1137-41. doi: 10.1126/science.1208227. Epub 2011 Jul 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of California, Irvine, CA 92697, USA. rreed@uci.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21778360" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Biological ; Animals ; *Biological Evolution ; Butterflies/anatomy & histology/*genetics/growth & development ; Evolution, Molecular ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; *Genes, Insect ; Genetic Variation ; Genome, Insect ; Homeodomain Proteins/*genetics ; Insect Proteins/*genetics ; Linkage Disequilibrium ; Molecular Sequence Data ; Moths/genetics ; Phenotype ; Pigmentation/*genetics ; Regulatory Elements, Transcriptional ; Selection, Genetic ; Species Specificity ; Transcription Factors/genetics ; Transcription, Genetic ; Wings, Animal/*anatomy & histology/growth & development
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    Model-driven engineering of RNA devices to quantitatively program gene expression (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-24
    Description: The models and simulation tools available to design functionally complex synthetic biological devices are very limited. We formulated a design-driven approach that used mechanistic modeling and kinetic RNA folding simulations to engineer RNA-regulated genetic devices that control gene expression. Ribozyme and metabolite-controlled, aptazyme-regulated expression devices with quantitatively predictable functions were assembled from components characterized in vitro, in vivo, and in silico. The models and design strategy were verified by constructing 28 Escherichia coli expression devices that gave excellent quantitative agreement between the predicted and measured gene expression levels (r = 0.94). These technologies were applied to engineer RNA-regulated controls in metabolic pathways. More broadly, we provide a framework for studying RNA functions and illustrate the potential for the use of biochemical and biophysical modeling to develop biological design methods.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carothers, James M -- Goler, Jonathan A -- Juminaga, Darmawi -- Keasling, Jay D -- New York, N.Y. -- Science. 2011 Dec 23;334(6063):1716-9. doi: 10.1126/science.1212209.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉California Institute for Quantitative Biosciences, University of California, Berkeley, Berkeley CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22194579" target="_blank"〉PubMed〈/a〉
    Keywords: Computer Simulation ; *Computer-Aided Design ; Escherichia coli/genetics/metabolism ; *Gene Expression Regulation ; Gene Regulatory Networks ; *Genetic Engineering ; Ligands ; Metabolic Networks and Pathways/genetics ; Models, Genetic ; Monte Carlo Method ; Nucleic Acid Conformation ; Phenylalanine/analogs & derivatives/metabolism ; RNA Folding ; RNA, Catalytic/chemistry/genetics/*metabolism ; Synthetic Biology ; Theophylline/metabolism ; Transcription, Genetic
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    Neuronal GPCR controls innate immunity by regulating noncanonical unfolded protein response genes (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-04-09
    Description: The unfolded protein response (UPR), which is activated when unfolded or misfolded proteins accumulate in the endoplasmic reticulum, has been implicated in the normal physiology of immune defense and in several human diseases, including diabetes, cancer, neurodegenerative disease, and inflammatory disease. In this study, we found that the nervous system controlled the activity of a noncanonical UPR pathway required for innate immunity in Caenorhabditis elegans. OCTR-1, a putative octopamine G protein-coupled catecholamine receptor (GPCR, G protein-coupled receptor), functioned in sensory neurons designated ASH and ASI to actively suppress innate immune responses by down-regulating the expression of noncanonical UPR genes pqn/abu in nonneuronal tissues. Our findings suggest a molecular mechanism by which the nervous system may sense inflammatory responses and respond by controlling stress-response pathways at the organismal level.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3125668/" 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/PMC3125668/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Jingru -- Singh, Varsha -- Kajino-Sakamoto, Rie -- Aballay, Alejandro -- GM070977/GM/NIGMS NIH HHS/ -- R01 GM070977/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 May 6;332(6030):729-32. doi: 10.1126/science.1203411. Epub 2011 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27705, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21474712" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Load ; Caenorhabditis elegans/*genetics/*immunology/microbiology ; Caenorhabditis elegans Proteins/genetics/metabolism/*physiology ; Down-Regulation ; Endoplasmic Reticulum/metabolism ; *Genes, Helminth ; *Immunity, Innate ; Intestines/metabolism ; Membrane Proteins/genetics/metabolism ; Mitogen-Activated Protein Kinases/genetics/metabolism ; Mutation ; Pharynx/metabolism ; Pseudomonas aeruginosa/*immunology/pathogenicity ; Receptors, G-Protein-Coupled/genetics/*physiology ; Sensory Receptor Cells/*physiology ; Signal Transduction ; Stress, Physiological ; Transcription, Genetic ; Unfolded Protein Response/*genetics ; Up-Regulation
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    The antiproliferative action of progesterone in uterine epithelium is mediated by Hand2 (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-02-19
    Description: During pregnancy, progesterone inhibits the growth-promoting actions of estrogen in the uterus. However, the mechanism for this is not clear. The attenuation of estrogen-mediated proliferation of the uterine epithelium by progesterone is a prerequisite for successful implantation. Our study reveals that progesterone-induced expression of the basic helix-loop-helix transcription factor Hand2 in the uterine stroma suppresses the production of several fibroblast growth factors (FGFs) that act as paracrine mediators of mitogenic effects of estrogen on the epithelium. In mouse uteri lacking Hand2, continued induction of these FGFs in the stroma maintains epithelial proliferation and stimulates estrogen-induced pathways, resulting in impaired implantation. Thus, Hand2 is a critical regulator of the uterine stromal-epithelial communication that directs proper steroid regulation conducive for the establishment of pregnancy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320855/" 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/PMC3320855/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Quanxi -- Kannan, Athilakshmi -- DeMayo, Francesco J -- Lydon, John P -- Cooke, Paul S -- Yamagishi, Hiroyuki -- Srivastava, Deepak -- Bagchi, Milan K -- Bagchi, Indrani C -- U54 HD055787-01A1/HD/NICHD NIH HHS/ -- U54HD055787/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 18;331(6019):912-6. doi: 10.1126/science.1197454.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Comparative Biosciences, University of Illinois Urbana/Champaign, Urbana, IL 61820, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21330545" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/*genetics/*metabolism ; Cell Proliferation ; Embryo Implantation/*physiology ; Endometrium/drug effects/*metabolism ; Epithelial Cells/cytology/drug effects/metabolism ; Epithelium/metabolism ; Estradiol/metabolism ; Estrogen Receptor alpha/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Fibroblast Growth Factors/genetics/*metabolism ; Gene Expression Profiling ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mifepristone/pharmacology ; Mucin-1/metabolism ; Phosphorylation ; Pregnancy ; Progesterone/antagonists & inhibitors/*metabolism/pharmacology ; Receptors, Fibroblast Growth Factor/metabolism ; Receptors, Progesterone/metabolism ; *Signal Transduction ; Stromal Cells/cytology/metabolism ; Transcription, Genetic
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    Transgenerational epigenetic instability is a source of novel methylation variants (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-09-17
    Description: Epigenetic information, which may affect an organism's phenotype, can be stored and stably inherited in the form of cytosine DNA methylation. Changes in DNA methylation can produce meiotically stable epialleles that affect transcription and morphology, but the rates of spontaneous gain or loss of DNA methylation are unknown. We examined spontaneously occurring variation in DNA methylation in Arabidopsis thaliana plants propagated by single-seed descent for 30 generations. We identified 114,287 CG single methylation polymorphisms and 2485 CG differentially methylated regions (DMRs), both of which show patterns of divergence compared with the ancestral state. Thus, transgenerational epigenetic variation in DNA methylation may generate new allelic states that alter transcription, providing a mechanism for phenotypic diversity in the absence of genetic mutation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210014/" 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/PMC3210014/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmitz, Robert J -- Schultz, Matthew D -- Lewsey, Mathew G -- O'Malley, Ronan C -- Urich, Mark A -- Libiger, Ondrej -- Schork, Nicholas J -- Ecker, Joseph R -- F32 HG004830/HG/NHGRI NIH HHS/ -- F32 HG004830-01/HG/NHGRI NIH HHS/ -- F32 HG004830-02/HG/NHGRI NIH HHS/ -- F32 HG004830-03/HG/NHGRI NIH HHS/ -- F32-HG004830/HG/NHGRI NIH HHS/ -- 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/ -- UL1 RR025774/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Oct 21;334(6054):369-73. doi: 10.1126/science.1212959. Epub 2011 Sep 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921155" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Arabidopsis/*genetics/metabolism ; *DNA Methylation ; DNA Transposable Elements ; DNA, Intergenic ; DNA, Plant/genetics/metabolism ; Dinucleoside Phosphates/metabolism ; *Epigenesis, Genetic ; Genes, Plant ; Genetic Variation ; Genome, Plant ; Linear Models ; Mutation ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Transcription, Genetic
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    TFEB links autophagy to lysosomal biogenesis (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-05-28
    Description: Autophagy is a cellular catabolic process that relies on the cooperation of autophagosomes and lysosomes. During starvation, the cell expands both compartments to enhance degradation processes. We found that starvation activates a transcriptional program that controls major steps of the autophagic pathway, including autophagosome formation, autophagosome-lysosome fusion, and substrate degradation. The transcription factor EB (TFEB), a master gene for lysosomal biogenesis, coordinated this program by driving expression of autophagy and lysosomal genes. Nuclear localization and activity of TFEB were regulated by serine phosphorylation mediated by the extracellular signal-regulated kinase 2, whose activity was tuned by the levels of extracellular nutrients. Thus, a mitogen-activated protein kinase-dependent mechanism regulates autophagy by controlling the biogenesis and partnership of two distinct cellular organelles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3638014/" 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/PMC3638014/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Settembre, Carmine -- Di Malta, Chiara -- Polito, Vinicia Assunta -- Garcia Arencibia, Moises -- Vetrini, Francesco -- Erdin, Serkan -- Erdin, Serpil Uckac -- Huynh, Tuong -- Medina, Diego -- Colella, Pasqualina -- Sardiello, Marco -- Rubinsztein, David C -- Ballabio, Andrea -- 250154/European Research Council/International -- 5 P30 HD024064/HD/NICHD NIH HHS/ -- G0600194/Medical Research Council/United Kingdom -- P30 HD024064/HD/NICHD NIH HHS/ -- R01 NS078072/NS/NINDS NIH HHS/ -- TGM11CB6/Telethon/Italy -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Jun 17;332(6036):1429-33. doi: 10.1126/science.1204592. Epub 2011 May 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Telethon Institute of Genetics and Medicine (TIGEM), Via Pietro Castellino 111, 80131 Naples, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21617040" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; *Autophagy ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics/*metabolism ; COS Cells ; Cell Nucleus/*metabolism ; Cells, Cultured ; Cercopithecus aethiops ; Cytoplasm/metabolism ; Gene Expression Regulation ; HeLa Cells ; Humans ; Liver/metabolism ; Lysosomes/*metabolism ; MAP Kinase Signaling System ; Mice ; Mice, Transgenic ; Microtubule-Associated Proteins/metabolism ; Mitogen-Activated Protein Kinase 1/metabolism ; Phagosomes/metabolism ; Phosphorylation ; RNA Interference ; Transcription, Genetic ; Up-Regulation
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    Mouse B-type lamins are required for proper organogenesis but not by embryonic stem cells (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-11-26
    Description: B-type lamins, the major components of the nuclear lamina, are believed to be essential for cell proliferation and survival. We found that mouse embryonic stem cells (ESCs) do not need any lamins for self-renewal and pluripotency. Although genome-wide lamin-B binding profiles correlate with reduced gene expression, such binding is not directly required for gene silencing in ESCs or trophectoderm cells. However, B-type lamins are required for proper organogenesis. Defects in spindle orientation in neural progenitor cells and migration of neurons probably cause brain disorganizations found in lamin-B null mice. Thus, our studies not only disprove several prevailing views of lamin-Bs but also establish a foundation for redefining the function of the nuclear lamina in the context of tissue building and homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306219/" 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/PMC3306219/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Youngjo -- Sharov, Alexei A -- McDole, Katie -- Cheng, Melody -- Hao, Haiping -- Fan, Chen-Ming -- Gaiano, Nicholas -- Ko, Minoru S H -- Zheng, Yixian -- R01 AR060042/AR/NIAMS NIH HHS/ -- R01 AR060042-02/AR/NIAMS NIH HHS/ -- R01 GM 56312/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Dec 23;334(6063):1706-10. doi: 10.1126/science.1211222. Epub 2011 Nov 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Embryology, Carnegie Institution for Science, Baltimore, MD 21218, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22116031" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Size ; Brain/cytology/embryology ; Cell Cycle ; Cell Differentiation ; Cell Movement ; Cells, Cultured ; Chromatin/metabolism ; Embryonic Development ; Embryonic Stem Cells/cytology/*physiology ; Female ; Gene Expression Regulation, Developmental ; Gene Silencing ; Lamin Type B/genetics/metabolism/*physiology ; Male ; Mice ; Mice, Knockout ; Neural Stem Cells/cytology ; Neurons/cytology ; Nuclear Lamina/physiology ; Organ Size ; *Organogenesis ; Pluripotent Stem Cells/cytology/physiology ; Promoter Regions, Genetic ; Spindle Apparatus/physiology/ultrastructure ; Transcription, Genetic ; Trophoblasts/cytology
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    Histone lysine demethylase JARID1a activates CLOCK-BMAL1 and influences the circadian clock (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-10-01
    Description: In animals, circadian oscillators are based on a transcription-translation circuit that revolves around the transcription factors CLOCK and BMAL1. We found that the JumonjiC (JmjC) and ARID domain-containing histone lysine demethylase 1a (JARID1a) formed a complex with CLOCK-BMAL1, which was recruited to the Per2 promoter. JARID1a increased histone acetylation by inhibiting histone deacetylase 1 function and enhanced transcription by CLOCK-BMAL1 in a demethylase-independent manner. Depletion of JARID1a in mammalian cells reduced Per promoter histone acetylation, dampened expression of canonical circadian genes, and shortened the period of circadian rhythms. Drosophila lines with reduced expression of the Jarid1a homolog, lid, had lowered Per expression and similarly altered circadian rhythms. JARID1a thus has a nonredundant role in circadian oscillator function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3204309/" 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/PMC3204309/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DiTacchio, Luciano -- Le, Hiep D -- Vollmers, Christopher -- Hatori, Megumi -- Witcher, Michael -- Secombe, Julie -- Panda, Satchidananda -- DK 091618/DK/NIDDK NIH HHS/ -- EY 16807/EY/NEI NIH HHS/ -- F32GM082083/GM/NIGMS NIH HHS/ -- R01 DK091618/DK/NIDDK NIH HHS/ -- R01 EY016807/EY/NEI NIH HHS/ -- S10 RR027450/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2011 Sep 30;333(6051):1881-5. doi: 10.1126/science.1206022.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regulatory Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21960634" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/*metabolism ; Acetylation ; Animals ; CLOCK Proteins/*metabolism ; *Circadian Clocks ; DNA-Binding Proteins ; Drosophila/genetics/physiology ; Drosophila Proteins/genetics/metabolism ; Gene Expression Regulation ; HEK293 Cells ; Histone Deacetylase Inhibitors ; Histone Deacetylases/metabolism ; Histone Demethylases ; Histone-Lysine N-Methyltransferase/genetics/metabolism ; Histones/metabolism ; Humans ; Jumonji Domain-Containing Histone Demethylases ; Male ; Mice ; Mice, Knockout ; Period Circadian Proteins/genetics ; Promoter Regions, Genetic ; Retinoblastoma-Binding Protein 2/*metabolism ; Transcription, Genetic ; Transfection
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    Quantifying E. coli proteome and transcriptome with single-molecule sensitivity in single cells (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-07-31
    Description: Protein and messenger RNA (mRNA) copy numbers vary from cell to cell in isogenic bacterial populations. However, these molecules often exist in low copy numbers and are difficult to detect in single cells. We carried out quantitative system-wide analyses of protein and mRNA expression in individual cells with single-molecule sensitivity using a newly constructed yellow fluorescent protein fusion library for Escherichia coli. We found that almost all protein number distributions can be described by the gamma distribution with two fitting parameters which, at low expression levels, have clear physical interpretations as the transcription rate and protein burst size. At high expression levels, the distributions are dominated by extrinsic noise. We found that a single cell's protein and mRNA copy numbers for any given gene are uncorrelated.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2922915/" 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/PMC2922915/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taniguchi, Yuichi -- Choi, Paul J -- Li, Gene-Wei -- Chen, Huiyi -- Babu, Mohan -- Hearn, Jeremy -- Emili, Andrew -- Xie, X Sunney -- DP1 OD000277/OD/NIH HHS/ -- DP1 OD000277-03/OD/NIH HHS/ -- DP1 OD000277-04/OD/NIH HHS/ -- DP1 OD000277-05/OD/NIH HHS/ -- MOP-77639/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2010 Jul 30;329(5991):533-8. doi: 10.1126/science.1188308.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671182" target="_blank"〉PubMed〈/a〉
    Keywords: Escherichia coli/chemistry/*genetics/metabolism ; Escherichia coli Proteins/*analysis/metabolism ; *Gene Expression ; *Gene Expression Profiling ; Gene Library ; In Situ Hybridization, Fluorescence ; Luminescent Proteins ; Microfluidic Analytical Techniques ; Microscopy, Fluorescence ; Protein Biosynthesis ; Proteome/*analysis ; RNA Stability ; RNA, Bacterial/analysis/genetics/metabolism ; RNA, Messenger/*analysis/genetics ; Saccharomyces cerevisiae/chemistry/genetics/metabolism ; Transcription, Genetic
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    Identification of RACK1 and protein kinase Calpha as integral components of the mammalian circadian clock (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-23
    Description: At the core of the mammalian circadian clock is a negative feedback loop in which the dimeric transcription factor CLOCK-BMAL1 drives processes that in turn suppress its transcriptional activity. To gain insight into the mechanisms of circadian feedback, we analyzed mouse protein complexes containing BMAL1. Receptor for activated C kinase-1 (RACK1) and protein kinase C-alpha (PKCalpha) were recruited in a circadian manner into a nuclear BMAL1 complex during the negative feedback phase of the cycle. Overexpression of RACK1 and PKCalpha suppressed CLOCK-BMAL1 transcriptional activity, and RACK1 stimulated phosphorylation of BMAL1 by PKCalpha in vitro. Depletion of endogenous RACK1 or PKCalpha from fibroblasts shortened the circadian period, demonstrating that both molecules function in the clock oscillatory mechanism. Thus, the classical PKC signaling pathway is not limited to relaying external stimuli but is rhythmically activated by internal processes, forming an integral part of the circadian feedback loop.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robles, Maria S -- Boyault, Cyril -- Knutti, Darko -- Padmanabhan, Kiran -- Weitz, Charles J -- New York, N.Y. -- Science. 2010 Jan 22;327(5964):463-6. doi: 10.1126/science.1180067.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093473" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/metabolism ; Animals ; CLOCK Proteins/metabolism ; Cell Nucleus/metabolism ; Circadian Rhythm/*physiology ; Feedback, Physiological ; Fibroblasts/metabolism/physiology ; Mice ; Mice, Inbred C57BL ; Neuropeptides/genetics/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinase C-alpha/*metabolism ; RNA Interference ; Signal Transduction ; Transcription, Genetic
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    Molecular signals of epigenetic states (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-30
    Description: Epigenetic signals are responsible for the establishment, maintenance, and reversal of metastable transcriptional states that are fundamental for the cell's ability to "remember" past events, such as changes in the external environment or developmental cues. Complex epigenetic states are orchestrated by several converging and reinforcing signals, including transcription factors, noncoding RNAs, DNA methylation, and histone modifications. Although all of these pathways modulate transcription from chromatin in vivo, the mechanisms by which epigenetic information is transmitted through cell division remain unclear. Because epigenetic states are metastable and change in response to the appropriate signals, a deeper understanding of their molecular framework will allow us to tackle the dysregulation of epigenetics in disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772643/" 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/PMC3772643/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonasio, Roberto -- Tu, Shengjiang -- Reinberg, Danny -- GM037120/GM/NIGMS NIH HHS/ -- GM064844/GM/NIGMS NIH HHS/ -- R01 GM064844/GM/NIGMS NIH HHS/ -- R37 GM037120/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Oct 29;330(6004):612-6. doi: 10.1126/science.1191078.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, School of Medicine, New York University, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21030644" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Chromatin/chemistry/genetics/metabolism ; *DNA Methylation ; *Epigenesis, Genetic ; Histones/*metabolism ; Humans ; Protein Processing, Post-Translational ; RNA, Untranslated/genetics/*metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic
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    Essential role of the histone methyltransferase G9a in cocaine-induced plasticity (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-09
    Description: Cocaine-induced alterations in gene expression cause changes in neuronal morphology and behavior that may underlie cocaine addiction. In mice, we identified an essential role for histone 3 lysine 9 (H3K9) dimethylation and the lysine dimethyltransferase G9a in cocaine-induced structural and behavioral plasticity. Repeated cocaine administration reduced global levels of H3K9 dimethylation in the nucleus accumbens. This reduction in histone methylation was mediated through the repression of G9a in this brain region, which was regulated by the cocaine-induced transcription factor DeltaFosB. Using conditional mutagenesis and viral-mediated gene transfer, we found that G9a down-regulation increased the dendritic spine plasticity of nucleus accumbens neurons and enhanced the preference for cocaine, thereby establishing a crucial role for histone methylation in the long-term actions of cocaine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820240/" 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/PMC2820240/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maze, Ian -- Covington, Herbert E 3rd -- Dietz, David M -- LaPlant, Quincey -- Renthal, William -- Russo, Scott J -- Mechanic, Max -- Mouzon, Ezekiell -- Neve, Rachael L -- Haggarty, Stephen J -- Ren, Yanhua -- Sampath, Srihari C -- Hurd, Yasmin L -- Greengard, Paul -- Tarakhovsky, Alexander -- Schaefer, Anne -- Nestler, Eric J -- P01 DA008227/DA/NIDA NIH HHS/ -- P01 DA008227-120001/DA/NIDA NIH HHS/ -- P01 DA008227-129001/DA/NIDA NIH HHS/ -- P01 DA008227-13/DA/NIDA NIH HHS/ -- P01 DA008227-14/DA/NIDA NIH HHS/ -- P01 DA008227-15/DA/NIDA NIH HHS/ -- P01 DA008227-16/DA/NIDA NIH HHS/ -- P01 DA008227-170003/DA/NIDA NIH HHS/ -- P01 DA008227-180003/DA/NIDA NIH HHS/ -- P01 DA010044/DA/NIDA NIH HHS/ -- P01 DA010044-14/DA/NIDA NIH HHS/ -- P01 DA010044-140005/DA/NIDA NIH HHS/ -- P01 DA010044-149002/DA/NIDA NIH HHS/ -- P01 DA010044-14S1/DA/NIDA NIH HHS/ -- P01 DA010044-14S10005/DA/NIDA NIH HHS/ -- P01 DA010044-14S19002/DA/NIDA NIH HHS/ -- P01 DA010044-15/DA/NIDA NIH HHS/ -- P01 DA010044-150005/DA/NIDA NIH HHS/ -- P01 DA010044-159002/DA/NIDA NIH HHS/ -- P01 DA08227/DA/NIDA NIH HHS/ -- P0110044/PHS HHS/ -- R01 DA007359/DA/NIDA NIH HHS/ -- R01 DA007359-02/DA/NIDA NIH HHS/ -- R01 DA007359-17/DA/NIDA NIH HHS/ -- R01 DA007359-18/DA/NIDA NIH HHS/ -- R01 DA007359-19/DA/NIDA NIH HHS/ -- R01 DA007359-20/DA/NIDA NIH HHS/ -- R01 DA007359-21/DA/NIDA NIH HHS/ -- R01 DA007359-22/DA/NIDA NIH HHS/ -- R01 DA014133/DA/NIDA NIH HHS/ -- R01 DA07359/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):213-6. doi: 10.1126/science.1179438.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20056891" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*drug effects ; Cocaine/*administration & dosage/pharmacology ; Cocaine-Related Disorders/etiology/metabolism ; Dendritic Spines/physiology ; Down-Regulation ; Enzyme Repression ; Gene Expression Profiling ; Gene Expression Regulation ; Histone-Lysine N-Methyltransferase/genetics/*metabolism ; Histones/*metabolism ; Lysine/metabolism ; Male ; Methylation ; Mice ; Mice, Inbred C57BL ; *Neuronal Plasticity ; Neurons/drug effects/*metabolism ; Nucleus Accumbens/cytology/drug effects/*metabolism ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins c-fos/genetics/metabolism ; Reward ; Self Administration ; Transcription, Genetic
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    The Lmo2 oncogene initiates leukemia in mice by inducing thymocyte self-renewal (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-23
    Description: The LMO2 oncogene causes a subset of human T cell acute lymphoblastic leukemias (T-ALL), including four cases that arose as adverse events in gene therapy trials. To investigate the cellular origin of LMO2-induced leukemia, we used cell fate mapping to study mice in which the Lmo2 gene was constitutively expressed in the thymus. Lmo2 induced self-renewal of committed T cells in the mice more than 8 months before the development of overt T-ALL. These self-renewing cells retained the capacity for T cell differentiation but expressed several genes typical of hematopoietic stem cells (HSCs), suggesting that Lmo2 might reactivate an HSC-specific transcriptional program. Forced expression of one such gene, Hhex, was sufficient to initiate self-renewal of thymocytes in vivo. Thus, Lmo2 promotes the self-renewal of preleukemic thymocytes, providing a mechanism by which committed T cells can then accumulate additional genetic mutations required for leukemic transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCormack, Matthew P -- Young, Lauren F -- Vasudevan, Sumitha -- de Graaf, Carolyn A -- Codrington, Rosalind -- Rabbitts, Terence H -- Jane, Stephen M -- Curtis, David J -- G0600914/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):879-83. doi: 10.1126/science.1182378. Epub 2010 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rotary Bone Marrow Research Laboratories, Royal Melbourne Hospital, Grattan Street, Parkville, Victoria 3050, Australia. mccormack@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093438" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Cell Differentiation ; Cell Transformation, Neoplastic/*genetics ; DNA-Binding Proteins/*genetics/metabolism ; Down-Regulation ; Gene Expression Profiling ; Gene Expression Regulation, Leukemic ; Homeodomain Proteins/genetics ; Humans ; LIM Domain Proteins ; Metalloproteins/*genetics/metabolism ; Mice ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; *Oncogenes ; Precursor Cells, T-Lymphoid/*physiology/transplantation ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/*genetics/metabolism/pathology ; Preleukemia/genetics/metabolism/pathology ; Proto-Oncogene Proteins ; T-Lymphocyte Subsets ; T-Lymphocytes/*physiology/transplantation ; Thymus Gland/metabolism/pathology ; Transcription Factors/genetics ; Transcription, Genetic ; Up-Regulation
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    GE Prize-winning essay. 2010 Grand Prize winner (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2010 Dec 3;330(6009):1335. doi: 10.1126/science.330.6009.1335.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127241" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Apoptosis ; *Awards and Prizes ; Biological Science Disciplines/history ; Canada ; Europe ; History, 21st Century ; Japan ; Microscopy, Fluorescence/*methods ; Singapore ; Transcription, Genetic
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    Vibrio cholerae VpsT regulates matrix production and motility by directly sensing cyclic di-GMP (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-13
    Description: Microorganisms can switch from a planktonic, free-swimming life-style to a sessile, colonial state, called a biofilm, which confers resistance to environmental stress. Conversion between the motile and biofilm life-styles has been attributed to increased levels of the prokaryotic second messenger cyclic di-guanosine monophosphate (c-di-GMP), yet the signaling mechanisms mediating such a global switch are poorly understood. Here we show that the transcriptional regulator VpsT from Vibrio cholerae directly senses c-di-GMP to inversely control extracellular matrix production and motility, which identifies VpsT as a master regulator for biofilm formation. Rather than being regulated by phosphorylation, VpsT undergoes a change in oligomerization on c-di-GMP binding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828054/" 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/PMC2828054/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krasteva, Petya V -- Fong, Jiunn C N -- Shikuma, Nicholas J -- Beyhan, Sinem -- Navarro, Marcos V A S -- Yildiz, Fitnat H -- Sondermann, Holger -- 1R01GM081373/GM/NIGMS NIH HHS/ -- P30 EB009998/EB/NIBIB NIH HHS/ -- R01 AI055987/AI/NIAID NIH HHS/ -- R01 AI055987-06A1/AI/NIAID NIH HHS/ -- R01 GM081373/GM/NIGMS NIH HHS/ -- R01 GM081373-03/GM/NIGMS NIH HHS/ -- R01AI055987/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):866-8. doi: 10.1126/science.1181185.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Medicine, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20150502" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Bacterial Proteins/chemistry/genetics/*metabolism ; Binding Sites ; Biofilms/*growth & development ; Crystallography, X-Ray ; Cyclic GMP/*analogs & derivatives/metabolism ; DNA, Bacterial/metabolism ; Dimerization ; Extracellular Matrix/*metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; Models, Molecular ; Movement ; Point Mutation ; Polysaccharides, Bacterial/genetics/metabolism ; Protein Folding ; Protein Multimerization ; Protein Structure, Tertiary ; Signal Transduction ; Transcription Factors/chemistry/genetics/*metabolism ; Transcription, Genetic ; Vibrio cholerae O1/cytology/genetics/*physiology
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    Direct restart of a replication fork stalled by a head-on RNA polymerase (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-30
    Description: In vivo studies suggest that replication forks are arrested by encounters with head-on transcription complexes. Yet, the fate of the replisome and RNA polymerase (RNAP) after a head-on collision is unknown. We found that the Escherichia coli replisome stalls upon collision with a head-on transcription complex, but instead of collapsing, the replication fork remains highly stable and eventually resumes elongation after displacing the RNAP from DNA. We also found that the transcription-repair coupling factor Mfd promotes direct restart of the fork after the collision by facilitating displacement of the RNAP. These findings demonstrate the intrinsic stability of the replication apparatus and a previously unknown role for the transcription-coupled repair pathway in promoting replication past a RNAP block.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2861996/" 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/PMC2861996/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pomerantz, Richard T -- O'Donnell, Mike -- R01 GM038839/GM/NIGMS NIH HHS/ -- R01 GM038839-23/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):590-2. doi: 10.1126/science.1179595.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Rockefeller University, Howard Hughes Medical Institute, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20110508" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/metabolism ; DNA Repair ; *DNA Replication ; DNA, Bacterial/*metabolism ; DNA-Directed DNA Polymerase/metabolism ; DNA-Directed RNA Polymerases/*metabolism ; Escherichia coli/genetics/*metabolism ; Escherichia coli Proteins/metabolism ; Templates, Genetic ; Transcription Factors/metabolism ; Transcription, Genetic
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    Regulation of oligodendrocyte differentiation and myelination (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-06
    Description: Despite the importance of myelin for the rapid conduction of action potentials, the molecular bases of oligodendrocyte differentiation and central nervous system (CNS) myelination are still incompletely understood. Recent results have greatly advanced this understanding, identifying new transcriptional regulators of myelin gene expression, elucidating vital roles for microRNAs in controlling myelination, and clarifying the extracellular signaling mechanisms that orchestrate the development of myelin. Studies have also demonstrated an unexpected level of plasticity of myelin in the adult CNS. These recent advances provide new insight into how remyelination may be stimulated in demyelinating disorders such as multiple sclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Emery, Ben -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):779-82. doi: 10.1126/science.1190927.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Neuroscience and Florey Neuroscience Institutes, Level 2, Alan Gilbert Building, The University of Melbourne, 161 Barry Street, Carlton South, Victoria 3053, Australia. emeryb@unimelb.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21051629" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cell Differentiation ; Central Nervous System/cytology/*physiology ; Chromatin Assembly and Disassembly ; Demyelinating Diseases/physiopathology/therapy ; Gene Expression Regulation ; Humans ; MicroRNAs/metabolism ; Myelin Sheath/*physiology ; Oligodendroglia/*cytology/*physiology ; Signal Transduction ; Transcription, Genetic
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    Phosphatidic acid is a pH biosensor that links membrane biogenesis to metabolism (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-08-28
    Description: Recognition of lipids by proteins is important for their targeting and activation in many signaling pathways, but the mechanisms that regulate such interactions are largely unknown. Here, we found that binding of proteins to the ubiquitous signaling lipid phosphatidic acid (PA) depended on intracellular pH and the protonation state of its phosphate headgroup. In yeast, a rapid decrease in intracellular pH in response to glucose starvation regulated binding of PA to a transcription factor, Opi1, that coordinately repressed phospholipid metabolic genes. This enabled coupling of membrane biogenesis to nutrient availability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, Barry P -- Shin, John J H -- Orij, Rick -- Chao, Jesse T -- Li, Shu Chen -- Guan, Xue Li -- Khong, Anthony -- Jan, Eric -- Wenk, Markus R -- Prinz, William A -- Smits, Gertien J -- Loewen, Christopher J R -- Canadian Institutes of Health Research/Canada -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1085-8. doi: 10.1126/science.1191026.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, British Columbia, V6T 1Z3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798321" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Cation Transport Proteins/genetics/metabolism ; Cell Membrane/*metabolism ; Cell Nucleus/metabolism ; Endoplasmic Reticulum/metabolism ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Glucose/metabolism ; Hydrogen-Ion Concentration ; Inositol/genetics/metabolism ; Liposomes/metabolism ; Mutation ; Phosphatidic Acids/*metabolism ; Protein Binding ; Protein Phosphatase 1/genetics/metabolism ; Proton-Translocating ATPases/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Saccharomyces cerevisiae/genetics/growth & development/*metabolism ; Saccharomyces cerevisiae Proteins/genetics/*metabolism ; Signal Transduction ; Transcription, Genetic ; Vacuolar Proton-Translocating ATPases/genetics/metabolism
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    Oscillating gene expression determines competence for periodic Arabidopsis root branching (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-09-11
    Description: Plants and animals produce modular developmental units in a periodic fashion. In plants, lateral roots form as repeating units along the root primary axis; however, the developmental mechanism regulating this process is unknown. We found that cyclic expression pulses of a reporter gene mark the position of future lateral roots by establishing prebranch sites and that prebranch site production and root bending are periodic. Microarray and promoter-luciferase studies revealed two sets of genes oscillating in opposite phases at the root tip. Genetic studies show that some oscillating transcriptional regulators are required for periodicity in one or both developmental processes. This molecular mechanism has characteristics that resemble molecular clock-driven activities in animal species.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2976612/" 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/PMC2976612/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moreno-Risueno, Miguel A -- Van Norman, Jaimie M -- Moreno, Antonio -- Zhang, Jingyuan -- Ahnert, Sebastian E -- Benfey, Philip N -- R01 GM043778/GM/NIGMS NIH HHS/ -- R01 GM043778-19/GM/NIGMS NIH HHS/ -- R01 GM043778-20/GM/NIGMS NIH HHS/ -- R01 GM043778-21/GM/NIGMS NIH HHS/ -- R01-GM043778/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1306-11. doi: 10.1126/science.1191937.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Institute for Genome Sciences and Policy Center for Systems Biology, Duke University, Durham, NC 27708, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829477" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/cytology/*genetics/*growth & development/metabolism ; Arabidopsis Proteins/genetics/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Plant ; Gene Regulatory Networks ; Genes, Plant ; Genes, Reporter ; Gravitation ; Indoleacetic Acids/metabolism/pharmacology ; Meristem/*genetics/*growth & development/metabolism ; Oligonucleotide Array Sequence Analysis ; Phthalimides/pharmacology ; Plant Roots/cytology/genetics/*growth & development ; Promoter Regions, Genetic ; Signal Transduction ; Temperature ; Time Factors ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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    Vernalization-mediated epigenetic silencing by a long intronic noncoding RNA (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-12-04
    Description: Vernalization is an environmentally-induced epigenetic switch in which winter cold triggers epigenetic silencing of floral repressors and thus provides competence to flower in spring. In Arabidopsis, winter cold triggers enrichment of tri-methylated histone H3 Lys(27) at chromatin of the floral repressor, FLOWERING LOCUS C (FLC), and results in epigenetically stable repression of FLC. This epigenetic change is mediated by an evolutionarily conserved repressive complex, polycomb repressive complex 2 (PRC2). Here, we show that a long intronic noncoding RNA [termed COLD ASSISTED INTRONIC NONCODING RNA (COLDAIR)] is required for the vernalization-mediated epigenetic repression of FLC. COLDAIR physically associates with a component of PRC2 and targets PRC2 to FLC. Our results show that COLDAIR is required for establishing stable repressive chromatin at FLC through its interaction with PRC2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heo, Jae Bok -- Sung, Sibum -- New York, N.Y. -- Science. 2011 Jan 7;331(6013):76-9. doi: 10.1126/science.1197349. Epub 2010 Dec 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular Cell and Developmental Biology and Institute for Cellular and Molecular Biology, the University of Texas at Austin, TX 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127216" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*genetics/growth & development/physiology ; Arabidopsis Proteins/*genetics/metabolism ; Carrier Proteins/metabolism ; Chromatin/metabolism ; *Cold Temperature ; DNA-Binding Proteins/genetics/metabolism ; *Epigenesis, Genetic ; Flowers/growth & development ; *Gene Expression Regulation, Plant ; *Gene Silencing ; Genes, Plant ; Histones/metabolism ; Homeodomain Proteins/metabolism ; Introns ; MADS Domain Proteins/*genetics/metabolism ; Nuclear Proteins/metabolism ; Plants, Genetically Modified ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; RNA Interference ; RNA Polymerase II/metabolism ; RNA, Antisense/genetics/metabolism ; RNA, Plant/genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; Recombinant Proteins/metabolism ; Repressor Proteins/metabolism ; Response Elements ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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    Neuroscience. Epigenetics and cognitive aging (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sweatt, J David -- New York, N.Y. -- Science. 2010 May 7;328(5979):701-2. doi: 10.1126/science.1189968.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Evelyn F. McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, AL 35294, USA. dsweatt@uab.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448174" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Aging/*genetics ; Animals ; Chromatin/metabolism ; *Chromatin Assembly and Disassembly ; *Epigenesis, Genetic ; Gene Expression Regulation ; Hippocampus/*metabolism ; Histone Deacetylase Inhibitors/pharmacology ; Histones/*metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Lysine/metabolism ; *Memory/drug effects ; Memory Disorders/*genetics/metabolism ; Mice ; Microfilament Proteins/genetics/metabolism ; Nuclear Proteins/genetics/metabolism ; Transcription, Genetic
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    Pathogenomics of Culex quinquefasciatus and meta-analysis of infection responses to diverse pathogens (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: The mosquito Culex quinquefasciatus poses a substantial threat to human and veterinary health as a primary vector of West Nile virus (WNV), the filarial worm Wuchereria bancrofti, and an avian malaria parasite. Comparative phylogenomics revealed an expanded canonical C. quinquefasciatus immune gene repertoire compared with those of Aedes aegypti and Anopheles gambiae. Transcriptomic analysis of C. quinquefasciatus genes responsive to WNV, W. bancrofti, and non-native bacteria facilitated an unprecedented meta-analysis of 25 vector-pathogen interactions involving arboviruses, filarial worms, bacteria, and malaria parasites, revealing common and distinct responses to these pathogen types in three mosquito genera. Our findings provide support for the hypothesis that mosquito-borne pathogens have evolved to evade innate immune responses in three vector mosquito species of major medical importance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104938/" 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/PMC3104938/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bartholomay, Lyric C -- Waterhouse, Robert M -- Mayhew, George F -- Campbell, Corey L -- Michel, Kristin -- Zou, Zhen -- Ramirez, Jose L -- Das, Suchismita -- Alvarez, Kanwal -- Arensburger, Peter -- Bryant, Bart -- Chapman, Sinead B -- Dong, Yuemei -- Erickson, Sara M -- Karunaratne, S H P Parakrama -- Kokoza, Vladimir -- Kodira, Chinnappa D -- Pignatelli, Patricia -- Shin, Sang Woon -- Vanlandingham, Dana L -- Atkinson, Peter W -- Birren, Bruce -- Christophides, George K -- Clem, Rollie J -- Hemingway, Janet -- Higgs, Stephen -- Megy, Karine -- Ranson, Hilary -- Zdobnov, Evgeny M -- Raikhel, Alexander S -- Christensen, Bruce M -- Dimopoulos, George -- Muskavitch, Marc A T -- F31 AI080161/AI/NIAID NIH HHS/ -- F31 AI080161-01A1/AI/NIAID NIH HHS/ -- HHSN266200400001C/AO/NIAID NIH HHS/ -- HHSN266200400001C/PHS HHS/ -- HHSN266200400039C/AI/NIAID NIH HHS/ -- HHSN266200400039C/PHS HHS/ -- P20 RR017686/RR/NCRR NIH HHS/ -- P20 RR017686-01/RR/NCRR NIH HHS/ -- R01 AI019769/AI/NIAID NIH HHS/ -- R01 AI019769-26/AI/NIAID NIH HHS/ -- R01 AI059492/AI/NIAID NIH HHS/ -- R01 AI059492-05/AI/NIAID NIH HHS/ -- R01 AI061576/AI/NIAID NIH HHS/ -- R01 AI061576-08/AI/NIAID NIH HHS/ -- R01 AI067698/AI/NIAID NIH HHS/ -- R01 AI067698-05/AI/NIAID NIH HHS/ -- R01 AI078997/AI/NIAID NIH HHS/ -- R01 AI078997-02/AI/NIAID NIH HHS/ -- R01 AI095842/AI/NIAID NIH HHS/ -- R01 AI19769/AI/NIAID NIH HHS/ -- R01 AI59492/AI/NIAID NIH HHS/ -- R01 AI67698/AI/NIAID NIH HHS/ -- R21 AI067642/AI/NIAID NIH HHS/ -- R21 AI067642-01/AI/NIAID NIH HHS/ -- T01CCT622892/PHS HHS/ -- T32 A107536/PHS HHS/ -- T32 AI007414/AI/NIAID NIH HHS/ -- T32 AI007417/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):88-90. doi: 10.1126/science.1193162.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Entomology, Iowa State University, Ames, IA 50011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929811" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/genetics/immunology/microbiology/parasitology ; Animals ; Anopheles gambiae/genetics/metabolism/microbiology/parasitology ; Arboviruses/immunology/pathogenicity/physiology ; Bacteria/immunology/pathogenicity ; Biological Evolution ; Culex/*genetics/*immunology/microbiology/parasitology ; Ecosystem ; Filarioidea/immunology/pathogenicity/physiology ; Gene Expression Profiling ; Gene Expression Regulation ; *Genes, Insect ; *Host-Pathogen Interactions ; Immunity, Innate/*genetics ; Insect Vectors/*genetics/*immunology/microbiology/parasitology ; Oligonucleotide Array Sequence Analysis ; Phylogeny ; RNA Interference ; Transcription, Genetic ; West Nile virus/immunology/pathogenicity/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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