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  • 1
    Publication Date: 2002-10-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michaels, David -- Bingham, Eula -- Boden, Les -- Clapp, Richard -- Goldman, Lynn R -- Hoppin, Polly -- Krimsky, Sheldon -- Monforton, Celeste -- Ozonoff, David -- Robbins, Anthony -- New York, N.Y. -- Science. 2002 Oct 25;298(5594):703.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12399550" target="_blank"〉PubMed〈/a〉
    Keywords: *Advisory Committees ; Biomedical Research ; Environmental Health ; *Federal Government ; Genetic Testing ; Politics ; *Science ; United States ; United States Dept. of Health and Human Services
    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
    Publication Date: 2010-07-16
    Description: Multiple pathways prevent DNA replication from occurring more than once per cell cycle. These pathways block re-replication by strictly controlling the activity of pre-replication complexes, which assemble at specific sites in the genome called origins. Here we show that mutations in the homologous histone 3 lysine 27 (H3K27) monomethyltransferases, ARABIDOPSIS TRITHORAX-RELATED PROTEIN5 (ATXR5) and ATXR6, lead to re-replication of specific genomic locations. Most of these locations correspond to transposons and other repetitive and silent elements of the Arabidopsis genome. These sites also correspond to high levels of H3K27 monomethylation, and mutation of the catalytic SET domain is sufficient to cause the re-replication defect. Mutation of ATXR5 and ATXR6 also causes upregulation of transposon expression and has pleiotropic effects on plant development. These results uncover a novel pathway that prevents over-replication of heterochromatin in Arabidopsis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2964344/" 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/PMC2964344/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacob, Yannick -- Stroud, Hume -- Leblanc, Chantal -- Feng, Suhua -- Zhuo, Luting -- Caro, Elena -- Hassel, Christiane -- Gutierrez, Crisanto -- Michaels, Scott D -- Jacobsen, Steven E -- GM075060/GM/NIGMS NIH HHS/ -- R01 GM075060/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Aug 19;466(7309):987-91. doi: 10.1038/nature09290. Epub 2010 Jul 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Indiana University, 915 East Third Street, Bloomington, Indiana 47405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20631708" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; *Arabidopsis/cytology/enzymology/genetics ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Catalytic Domain/genetics ; DNA Methylation ; DNA Replication/genetics/*physiology ; DNA Transposable Elements/genetics ; DNA, Plant/analysis/biosynthesis ; Gene Expression Regulation, Plant ; Gene Silencing ; Genome, Plant/genetics ; Heterochromatin/*genetics/metabolism ; Histone-Lysine N-Methyltransferase/*metabolism ; Histones/chemistry/*metabolism ; Lysine/metabolism ; Methylation ; Methyltransferases/chemistry/genetics/*metabolism ; Mutant Proteins/genetics/metabolism ; Mutation ; Replication Origin
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2003-11-01
    Description: The Arabidopsis autonomous floral-promotion pathway promotes flowering independently of the photoperiod and vernalization pathways by repressing FLOWERING LOCUS C (FLC), a MADS-box transcription factor that blocks the transition from vegetative to reproductive development. Here, we report that FLOWERING LOCUS D (FLD), one of six genes in the autonomous pathway, encodes a plant homolog of a protein found in histone deacetylase complexes in mammals. Lesions in FLD result in hyperacetylation of histones in FLC chromatin, up-regulation of FLC expression, and extremely delayed flowering. Thus, the autonomous pathway regulates flowering in part by histone deacetylation. However, not all autonomous-pathway mutants exhibit FLC hyperacetylation, indicating that multiple means exist by which this pathway represses FLC expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Yuehui -- Michaels, Scott D -- Amasino, Richard M -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1751-4. Epub 2003 Oct 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593187" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Amino Acid Sequence ; Arabidopsis/genetics/*growth & development/metabolism ; Arabidopsis Proteins/chemistry/*genetics/*metabolism ; Chromatin/metabolism ; Flowers/*growth & development ; Gene Expression Regulation, Plant ; Genes, Plant ; Histone Deacetylases/chemistry/genetics/*metabolism ; Histones/*metabolism ; Humans ; Introns ; MADS Domain Proteins/chemistry/*genetics/*metabolism ; Molecular Sequence Data ; Mutation ; Phenotype ; Plants, Genetically Modified ; Precipitin Tests ; Protein Structure, Tertiary ; Regulatory Sequences, Nucleic Acid ; Repressor Proteins/chemistry/metabolism ; Sequence Deletion ; 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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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michaels, David -- Wagner, Wendy -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2073.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Environmental and Occupational Health, George Washington University School of Public Health and Health Services, Washington, DC, 20052, USA. eohdmm@gwumc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684806" target="_blank"〉PubMed〈/a〉
    Keywords: Confidentiality ; *Conflict of Interest ; *Disclosure ; *Government Regulation ; *Private Sector ; Public Policy ; Research/*standards ; Research Support as Topic ; United States ; *United States Government Agencies
    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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  • 5
    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
    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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  • 6
    Publication Date: 2014-03-15
    Description: Histone variants have been proposed to act as determinants for posttranslational modifications with widespread regulatory functions. We identify a histone-modifying enzyme that selectively methylates the replication-dependent histone H3 variant H3.1. The crystal structure of the SET domain of the histone H3 lysine-27 (H3K27) methyltransferase ARABIDOPSIS TRITHORAX-RELATED PROTEIN 5 (ATXR5) in complex with a H3.1 peptide shows that ATXR5 contains a bipartite catalytic domain that specifically "reads" alanine-31 of H3.1. Variation at position 31 between H3.1 and replication-independent H3.3 is conserved in plants and animals, and threonine-31 in H3.3 is responsible for inhibiting the activity of ATXR5 and its paralog, ATXR6. Our results suggest a simple model for the mitotic inheritance of the heterochromatic mark H3K27me1 and the protection of H3.3-enriched genes against heterochromatization during DNA replication.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4049228/" 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/PMC4049228/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacob, Yannick -- Bergamin, Elisa -- Donoghue, Mark T A -- Mongeon, Vanessa -- LeBlanc, Chantal -- Voigt, Philipp -- Underwood, Charles J -- Brunzelle, Joseph S -- Michaels, Scott D -- Reinberg, Danny -- Couture, Jean-Francois -- Martienssen, Robert A -- BMA-355900/Canadian Institutes of Health Research/Canada -- GM064844/GM/NIGMS NIH HHS/ -- GM067014/GM/NIGMS NIH HHS/ -- GM075060/GM/NIGMS NIH HHS/ -- R01 GM067014/GM/NIGMS NIH HHS/ -- R01 GM075060/GM/NIGMS NIH HHS/ -- R37 GM037120/GM/NIGMS NIH HHS/ -- R37GM037120/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Mar 14;343(6176):1249-53. doi: 10.1126/science.1248357.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Watson School of Biological Sciences, Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24626927" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/genetics/*metabolism ; Arabidopsis Proteins/*chemistry/metabolism ; Catalytic Domain ; Conserved Sequence ; Crystallography, X-Ray ; DNA Replication ; Epigenesis, Genetic ; Gene Expression Regulation, Plant ; Heterochromatin/*metabolism ; Histones/*metabolism ; Methylation ; Methyltransferases/*chemistry/metabolism ; Mitosis ; Molecular Sequence Data ; *Protein Processing, Post-Translational ; Threonine/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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  • 7
    Publication Date: 2017-01-11
    Description: Previously, we have shown that loss of the histone 3 lysine 27 (H3K27) monomethyltransferases ARABIDOPSIS TRITHORAX-RELATED 5 (ATXR5) and ATXR6 (ATXR6) results in the overreplication of heterochromatin. Here we show that the overreplication results in DNA damage and extensive chromocenter remodeling into unique structures we have named “overreplication-associated centers” (RACs)....
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 8
    Publication Date: 1990-11-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 9
    Publication Date: 1976-08-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 10
    Publication Date: 1991-11-01
    Print ISSN: 0143-0807
    Electronic ISSN: 1361-6404
    Topics: Physics
    Published by Institute of Physics
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