<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Menon DU</submitter><funding>NCI NIH HHS</funding><funding>National Institute of General Medical Sciences</funding><funding>NIGMS NIH HHS</funding><pagination>RP88024</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11594533</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12</volume><pubmed_abstract>We present evidence implicating the BAF (BRG1/BRM Associated Factor) chromatin remodeler in meiotic sex chromosome inactivation (MSCI). By immunofluorescence (IF), the putative BAF DNA binding subunit, ARID1A (AT-rich Interaction Domain 1 a), appeared enriched on the male sex chromosomes during diplonema of meiosis I. Germ cells showing a Cre-induced loss of ARID1A arrested in pachynema and failed to repress sex-linked genes, indicating a defective MSCI. Mutant sex chromosomes displayed an abnormal presence of elongating RNA polymerase II coupled with an overall increase in chromatin accessibility detectable by ATAC-seq. We identified a role for ARID1A in promoting the preferential enrichment of the histone variant, H3.3, on the sex chromosomes, a known hallmark of MSCI. Without ARID1A, th</pubmed_abstract><journal>eLife</journal><pubmed_title>ARID1A governs the silencing of sex-linked transcription during male meiosis in the mouse.</pubmed_title><pmcid>PMC11594533</pmcid><funding_grant_id>P30 CA016086</funding_grant_id><funding_grant_id>R01GM101974</funding_grant_id><funding_grant_id>R01 GM101974</funding_grant_id><pubmed_authors>Magnuson T</pubmed_authors><pubmed_authors>Chakraborty P</pubmed_authors><pubmed_authors>Menon DU</pubmed_authors><pubmed_authors>Murcia N</pubmed_authors></additional><is_claimable>false</is_claimable><name>ARID1A governs the silencing of sex-linked transcription during male meiosis in the mouse.</name><description>We present evidence implicating the BAF (BRG1/BRM Associated Factor) chromatin remodeler in meiotic sex chromosome inactivation (MSCI). By immunofluorescence (IF), the putative BAF DNA binding subunit, ARID1A (AT-rich Interaction Domain 1 a), appeared enriched on the male sex chromosomes during diplonema of meiosis I. Germ cells showing a Cre-induced loss of ARID1A arrested in pachynema and failed to repress sex-linked genes, indicating a defective MSCI. Mutant sex chromosomes displayed an abnormal presence of elongating RNA polymerase II coupled with an overall increase in chromatin accessibility detectable by ATAC-seq. We identified a role for ARID1A in promoting the preferential enrichment of the histone variant, H3.3, on the sex chromosomes, a known hallmark of MSCI. Without ARID1A, th</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Nov</publication><modification>2026-06-01T13:24:05.036Z</modification><creation>2025-04-04T22:47:50.913Z</creation></dates><accession>S-EPMC11594533</accession><cross_references><pubmed>39589400</pubmed><doi>10.7554/eLife.88024</doi></cross_references></HashMap>