ATRX binds to atypical chromatin domains at the 3’ exons of ZNF genes to preserve H3K9me3 enrichment
نویسندگان
چکیده
Departments of Oncological Sciences and Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Instituto de Fisiología Celular, Departamento de Genética Molecular, Universidad Nacional Autónoma de México, México DF 04510, México. Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Department of Developmental Neurobiology, St Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA. Corresponding Author Correspondence and requests for materials should be addressed to Emily Bernstein, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, Room S6-114, New York, NY 10029, Phone: 212-824-9335, [email protected]
منابع مشابه
ATRX binds to atypical chromatin domains at the 3′ exons of zinc finger genes to preserve H3K9me3 enrichment
ATRX is a SWI/SNF chromatin remodeler proposed to govern genomic stability through the regulation of repetitive sequences, such as rDNA, retrotransposons, and pericentromeric and telomeric repeats. However, few direct ATRX target genes have been identified and high-throughput genomic approaches are currently lacking for ATRX. Here we present a comprehensive ChIP-sequencing study of ATRX in mult...
متن کاملCharacterization of the Contradictory Chromatin Signatures at the 3′ Exons of Zinc Finger Genes
The H3K9me3 histone modification is often found at promoter regions, where it functions to repress transcription. However, we have previously shown that 3' exons of zinc finger genes (ZNFs) are marked by high levels of H3K9me3. We have now further investigated this unusual location for H3K9me3 in ZNF genes. Neither bioinformatic nor experimental approaches support the hypothesis that the 3' exo...
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Mutations in the ATRX protein are associated with the alpha-thalassemia and mental retardation X-linked syndrome (ATR-X). Almost half of the disease-causing mutations occur in its ATRX-Dnmt3-Dnmt3L (ADD) domain. By employing peptide arrays, chromatin pull-down and peptide binding assays, we show specific binding of the ADD domain to H3 histone tail peptides containing H3K9me3. Peptide binding w...
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Genome-wide disruption of the epigenetic code is a hallmark of malignancy that encompasses many distinct, highly interactive modifications. Delineating the aberrant epigenome produced during toxicant-mediated malignant transformation will help identify the underlying epigenetic drivers of environmental toxicant-induced carcinogenesis. Gene promoter DNA methylation and gene expression profiling ...
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ATRX and MeCP2 belong to an expanding group of chromatin-associated proteins implicated in human neurodevelopmental disorders, although their gene-regulatory activities are not fully resolved. Loss of ATRX prevents full repression of an imprinted gene network in the postnatal brain and in this study we address the mechanistic aspects of this regulation. We show that ATRX binds many imprinted do...
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