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  • 1
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    Shotgun bisulphite sequencing of the Arabidopsis genome reveals DNA methylation patterning (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-02-19
    Beschreibung: Cytosine DNA methylation is important in regulating gene expression and in silencing transposons and other repetitive sequences. Recent genomic studies in Arabidopsis thaliana have revealed that many endogenous genes are methylated either within their promoters or within their transcribed regions, and that gene methylation is highly correlated with transcription levels. However, plants have different types of methylation controlled by different genetic pathways, and detailed information on the methylation status of each cytosine in any given genome is lacking. To this end, we generated a map at single-base-pair resolution of methylated cytosines for Arabidopsis, by combining bisulphite treatment of genomic DNA with ultra-high-throughput sequencing using the Illumina 1G Genome Analyser and Solexa sequencing technology. This approach, termed BS-Seq, unlike previous microarray-based methods, allows one to sensitively measure cytosine methylation on a genome-wide scale within specific sequence contexts. Here we describe methylation on previously inaccessible components of the genome and analyse the DNA methylation sequence composition and distribution. We also describe the effect of various DNA methylation mutants on genome-wide methylation patterns, and demonstrate that our newly developed library construction and computational methods can be applied to large genomes such as that of mouse.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2377394/" 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/PMC2377394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cokus, Shawn J -- Feng, Suhua -- Zhang, Xiaoyu -- Chen, Zugen -- Merriman, Barry -- Haudenschild, Christian D -- Pradhan, Sriharsa -- Nelson, Stanley F -- Pellegrini, Matteo -- Jacobsen, Steven E -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Mar 13;452(7184):215-9. doi: 10.1038/nature06745. Epub 2008 Feb 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cell, and Developmental Biology, University of California at Los Angeles, Los Angeles, California 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18278030" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 5-Methylcytosine/metabolism ; Animals ; Arabidopsis/*genetics ; Base Sequence ; Computational Biology ; Cytosine/metabolism ; *DNA Methylation ; Gene Expression Regulation, Plant/genetics ; Gene Library ; Genome, Plant/*genetics ; Mice ; Mutation/genetics ; Promoter Regions, Genetic/genetics ; Reproducibility of Results ; Sequence Analysis, DNA/*methods ; Sulfites/*metabolism ; Uracil/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    NLRX1 is a regulator of mitochondrial antiviral immunity (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-01-18
    Beschreibung: The RIG-like helicase (RLH) family of intracellular receptors detect viral nucleic acid and signal through the mitochondrial antiviral signalling adaptor MAVS (also known as Cardif, VISA and IPS-1) during a viral infection. MAVS activation leads to the rapid production of antiviral cytokines, including type 1 interferons. Although MAVS is vital to antiviral immunity, its regulation from within the mitochondria remains unknown. Here we describe human NLRX1, a highly conserved nucleotide-binding domain (NBD)- and leucine-rich-repeat (LRR)-containing family member (known as NLR) that localizes to the mitochondrial outer membrane and interacts with MAVS. Expression of NLRX1 results in the potent inhibition of RLH- and MAVS-mediated interferon-beta promoter activity and in the disruption of virus-induced RLH-MAVS interactions. Depletion of NLRX1 with small interference RNA promotes virus-induced type I interferon production and decreases viral replication. This work identifies NLRX1 as a check against mitochondrial antiviral responses and represents an intersection of three ancient cellular processes: NLR signalling, intracellular virus detection and the use of mitochondria as a platform for anti-pathogen signalling. This represents a conceptual advance, in that NLRX1 is a modulator of pathogen-associated molecular pattern receptors rather than a receptor, and identifies a key therapeutic target for enhancing antiviral responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, Chris B -- Bergstralh, Daniel T -- Duncan, Joseph A -- Lei, Yu -- Morrison, Thomas E -- Zimmermann, Albert G -- Accavitti-Loper, Mary A -- Madden, Victoria J -- Sun, Lijun -- Ye, Zhengmao -- Lich, John D -- Heise, Mark T -- Chen, Zhijian -- Ting, Jenny P-Y -- England -- Nature. 2008 Jan 31;451(7178):573-7. doi: 10.1038/nature06501. Epub 2008 Jan 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology-Immunology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18200010" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptor Proteins, Signal Transducing/antagonists & inhibitors/metabolism ; Animals ; Cell Line ; Cloning, Molecular ; Computational Biology ; Humans ; Interferon-beta/biosynthesis/genetics/metabolism ; Mice ; Mitochondria/*immunology/*metabolism ; Mitochondrial Membranes/metabolism ; Mitochondrial Proteins/genetics/*metabolism ; NF-kappa B/metabolism ; Protein Binding ; Protein Transport ; RNA, Small Interfering/genetics/metabolism ; Signal Transduction ; Virus Replication ; Viruses/*immunology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    ETS rearrangements and prostate cancer initiation (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-02-13
    Beschreibung: The first recurrent translocation event in prostate cancer has been recently described; it results in the translocation of an ETS (E26 transformation specific) transcription factor (ERG or ETV1) to the TMPRSS2 promoter region, which contains androgen responsive elements. The TMPRSS2:ERG genetic rearrangement has been reported to occur in approximately 40% of primary prostate tumours (ETV1 genetic rearrangements occur at a much lower frequency), and it results in the aberrant androgen-regulated expression of ERG. Tomlins et al. concluded that ETS genetic rearrangements are sufficient to initiate prostate neoplasia. However, here we show that ETS genetic rearrangements may in fact represent progression events rather than initiation events in prostate tumorigenesis. To this end, we demonstrate that the prostate-specific overexpression of ERG does not initiate prostate tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967456/" 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/PMC2967456/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carver, Brett S -- Tran, Jennifer -- Chen, Zhenbang -- Carracedo-Perez, Arkaitz -- Alimonti, Andrea -- Nardella, Caterina -- Gopalan, Anuradha -- Scardino, Peter T -- Cordon-Cardo, Carlos -- Gerald, William -- Pandolfi, Pier Paolo -- P50 CA092629/CA/NCI NIH HHS/ -- P50 CA092629-10/CA/NCI NIH HHS/ -- R01 CA082328/CA/NCI NIH HHS/ -- R01 CA082328-12/CA/NCI NIH HHS/ -- R01 MD004038/MD/NIMHD NIH HHS/ -- U01 CA084292/CA/NCI NIH HHS/ -- U01 CA084292-10/CA/NCI NIH HHS/ -- England -- Nature. 2009 Feb 12;457(7231):E1; discussion E2-3. doi: 10.1038/nature07738.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19212347" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Transformation, Neoplastic/*genetics/metabolism/pathology ; DNA-Binding Proteins/genetics ; Disease Progression ; Gene Expression ; Male ; Mice ; Mice, Transgenic ; Oncogene Proteins/genetics/metabolism ; Prostatic Neoplasms/*genetics/metabolism ; Transcription Factors/genetics ; *Translocation, Genetic
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    E2f1-3 switch from activators in progenitor cells to repressors in differentiating cells (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-12-18
    Beschreibung: In the established model of mammalian cell cycle control, the retinoblastoma protein (Rb) functions to restrict cells from entering S phase by binding and sequestering E2f activators (E2f1, E2f2 and E2f3), which are invariably portrayed as the ultimate effectors of a transcriptional program that commit cells to enter and progress through S phase. Using a panel of tissue-specific cre-transgenic mice and conditional E2f alleles we examined the effects of E2f1, E2f2 and E2f3 triple deficiency in murine embryonic stem cells, embryos and small intestines. We show that in normal dividing progenitor cells E2f1-3 function as transcriptional activators, but contrary to the current view, are dispensable for cell division and instead are necessary for cell survival. In differentiating cells E2f1-3 function in a complex with Rb as repressors to silence E2f targets and facilitate exit from the cell cycle. The inactivation of Rb in differentiating cells resulted in a switch of E2f1-3 from repressors to activators, leading to the superactivation of E2f responsive targets and ectopic cell divisions. Loss of E2f1-3 completely suppressed these phenotypes caused by Rb deficiency. This work contextualizes the activator versus repressor functions of E2f1-3 in vivo, revealing distinct roles in dividing versus differentiating cells and in normal versus cancer-like cell cycles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806193/" 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/PMC2806193/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chong, Jean-Leon -- Wenzel, Pamela L -- Saenz-Robles, M Teresa -- Nair, Vivek -- Ferrey, Antoney -- Hagan, John P -- Gomez, Yorman M -- Sharma, Nidhi -- Chen, Hui-Zi -- Ouseph, Madhu -- Wang, Shu-Huei -- Trikha, Prashant -- Culp, Brian -- Mezache, Louise -- Winton, Douglas J -- Sansom, Owen J -- Chen, Danian -- Bremner, Rod -- Cantalupo, Paul G -- Robinson, Michael L -- Pipas, James M -- Leone, Gustavo -- 5 T32 CA106196-04/CA/NCI NIH HHS/ -- CA098956/CA/NCI NIH HHS/ -- P01CA097189/CA/NCI NIH HHS/ -- R01 CA098956/CA/NCI NIH HHS/ -- R01 CA098956-06A2/CA/NCI NIH HHS/ -- R01CA82259/CA/NCI NIH HHS/ -- R01CA85619/CA/NCI NIH HHS/ -- R01HD04470/HD/NICHD NIH HHS/ -- England -- Nature. 2009 Dec 17;462(7275):930-4. doi: 10.1038/nature08677.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Virology, Immunology and Medical Genetics, College of Medicine, The Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016602" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Animals ; Apoptosis ; Cell Cycle/genetics/physiology ; *Cell Differentiation ; Cell Proliferation ; E2F Transcription Factors/deficiency/genetics/*metabolism ; E2F1 Transcription Factor/deficiency/genetics/metabolism ; E2F2 Transcription Factor/deficiency/genetics/metabolism ; E2F3 Transcription Factor/deficiency/genetics/metabolism ; Embryo, Mammalian/cytology/metabolism ; Embryonic Stem Cells/*cytology/*metabolism ; Female ; *Gene Expression Regulation ; Intestine, Small/cytology/metabolism ; Mice ; Mice, Transgenic ; Repressor Proteins/deficiency/genetics/*metabolism ; Retinoblastoma Protein/deficiency/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Dynamic visualization of thrombopoiesis within bone marrow (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2007-09-22
    Beschreibung: Platelets are generated from megakaryocytes (MKs) in mammalian bone marrow (BM) by mechanisms that remain poorly understood. Here we describe the use of multiphoton intravital microscopy in intact BM to visualize platelet generation in mice. MKs were observed as sessile cells that extended dynamic proplatelet-like protrusions into microvessels. These intravascular extensions appeared to be sheared from their transendothelial stems by flowing blood, resulting in the appearance of proplatelets in peripheral blood. In vitro, proplatelet production from differentiating MKs was enhanced by fluid shear. These results confirm the concept of proplatelet formation in vivo and are consistent with the possibility that blood flow-induced hydrodynamic shear stress is a biophysical determinant of thrombopoiesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Junt, Tobias -- Schulze, Harald -- Chen, Zhao -- Massberg, Steffen -- Goerge, Tobias -- Krueger, Andreas -- Wagner, Denisa D -- Graf, Thomas -- Italiano, Joseph E Jr -- Shivdasani, Ramesh A -- von Andrian, Ulrich H -- HL068130/HL/NHLBI NIH HHS/ -- HL56949/HL/NHLBI NIH HHS/ -- HL63143/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 21;317(5845):1767-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Disease Institute and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17885137" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Bacterial Proteins ; Blood Platelets/*cytology ; Bone Marrow/*physiology ; Cells, Cultured ; Luminescent Proteins ; Megakaryocytes/*cytology ; Mice ; Microscopy, Fluorescence, Multiphoton ; Platelet Membrane Glycoprotein IIb ; Shear Strength ; Thrombopoiesis/*physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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