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  • 1
    Publication Date: 2010-03-26
    Description: After fertilization the embryonic genome is inactive until transcription is initiated during the maternal-zygotic transition. This transition coincides with the formation of pluripotent cells, which in mammals can be used to generate embryonic stem cells. To study the changes in chromatin structure that accompany pluripotency and genome activation, we mapped the genomic locations of histone H3 molecules bearing lysine trimethylation modifications before and after the maternal-zygotic transition in zebrafish. Histone H3 lysine 27 trimethylation (H3K27me3), which is repressive, and H3K4me3, which is activating, were not detected before the transition. After genome activation, more than 80% of genes were marked by H3K4me3, including many inactive developmental regulatory genes that were also marked by H3K27me3. Sequential chromatin immunoprecipitation demonstrated that the same promoter regions had both trimethylation marks. Such bivalent chromatin domains also exist in embryonic stem cells and are thought to poise genes for activation while keeping them repressed. Furthermore, we found many inactive genes that were uniquely marked by H3K4me3. Despite this activating modification, these monovalent genes were neither expressed nor stably bound by RNA polymerase II. Inspection of published data sets revealed similar monovalent domains in embryonic stem cells. Moreover, H3K4me3 marks could form in the absence of both sequence-specific transcriptional activators and stable association of RNA polymerase II, as indicated by the analysis of an inducible transgene. These results indicate that bivalent and monovalent domains might poise embryonic genes for activation and that the chromatin profile associated with pluripotency is established during the maternal-zygotic transition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874748/" 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/PMC2874748/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vastenhouw, Nadine L -- Zhang, Yong -- Woods, Ian G -- Imam, Farhad -- Regev, Aviv -- Liu, X Shirley -- Rinn, John -- Schier, Alexander F -- 1R01 HG004069/HG/NHGRI NIH HHS/ -- 5R01 GM56211/GM/NIGMS NIH HHS/ -- DP1 OD003958/OD/NIH HHS/ -- R01 GM056211/GM/NIGMS NIH HHS/ -- R01 GM056211-11/GM/NIGMS NIH HHS/ -- R01 GM056211-12/GM/NIGMS NIH HHS/ -- R01 GM056211-12S1/GM/NIGMS NIH HHS/ -- R01 GM056211-13/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Apr 8;464(7290):922-6. doi: 10.1038/nature08866. Epub 2010 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20336069" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/*genetics/*metabolism ; Chromatin Immunoprecipitation ; *Gene Expression Regulation, Developmental/genetics ; Gene Silencing ; Genome/*genetics ; Histones/chemistry/metabolism ; Lysine/metabolism ; Methylation ; Oligonucleotide Array Sequence Analysis ; Pluripotent Stem Cells/*metabolism ; Promoter Regions, Genetic/genetics ; RNA Polymerase II/metabolism ; Transcriptional Activation ; Transgenes ; Zebrafish/*embryology/*genetics/metabolism ; Zebrafish Proteins/genetics ; Zygote/cytology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2007-04-21
    Description: Maternal gene products drive early development when the newly formed embryo is transcriptionally inactive. During the maternal-zygotic transition, embryonic transcription is initiated and many maternal RNAs are degraded. Multiple mechanisms regulate the birth of zygotic RNAs and the death of maternal RNAs. Genome activation appears to rely in part on the sequestration of transcriptional repressors by the exponentially increasing amount of DNA during cleavage divisions. Maternal RNA degradation is induced by the binding of proteins and microRNAs to the 3' untranslated region of target RNAs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schier, Alexander F -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):406-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard Stem Cell Institute, Center for Brain Science, Broad Institute, Harvard University, 16 Divinity Avenue, Room 1027, Cambridge, MA 02138, USA. schier@fas.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446392" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Cell Cycle ; Embryonic Development ; Female ; *Gene Expression Regulation, Developmental ; Gene Silencing ; MicroRNAs ; *RNA Stability ; RNA, Messenger/*metabolism ; RNA, Messenger, Stored/*metabolism ; RNA-Binding Proteins/metabolism ; Transcription, Genetic ; Zygote/cytology/*metabolism
    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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  • 3
    Publication Date: 2005-03-19
    Description: MicroRNAs (miRNAs) are small RNAs that regulate gene expression posttranscriptionally. To block all miRNA formation in zebrafish, we generated maternal-zygotic dicer (MZdicer) mutants that disrupt the Dicer ribonuclease III and double-stranded RNA-binding domains. Mutant embryos do not process precursor miRNAs into mature miRNAs, but injection of preprocessed miRNAs restores gene silencing, indicating that the disrupted domains are dispensable for later steps in silencing. MZdicer mutants undergo axis formation and differentiate multiple cell types but display abnormal morphogenesis during gastrulation, brain formation, somitogenesis, and heart development. Injection of miR-430 miRNAs rescues the brain defects in MZdicer mutants, revealing essential roles for miRNAs during morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giraldez, Antonio J -- Cinalli, Ryan M -- Glasner, Margaret E -- Enright, Anton J -- Thomson, J Michael -- Baskerville, Scott -- Hammond, Scott M -- Bartel, David P -- Schier, Alexander F -- New York, N.Y. -- Science. 2005 May 6;308(5723):833-8. Epub 2005 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Genetics Program, Skirball Institute of Biomolecular Medicine and Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA. giraldez@saturn.med.nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774722" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; Brain/*embryology ; Cell Differentiation ; Central Nervous System/embryology ; Gastrula/physiology ; Gene Silencing ; Heart/embryology ; MicroRNAs/genetics/metabolism/*physiology ; *Morphogenesis ; Mutation ; Neurons/cytology ; Phenotype ; RNA Processing, Post-Transcriptional ; RNA, Double-Stranded/metabolism ; Ribonuclease III/genetics/metabolism ; Signal Transduction ; Somites/cytology/physiology ; Spinal Cord/embryology ; Zebrafish/*embryology/*genetics
    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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