{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Menon DU"],"funding":["NCI NIH HHS","National Institute of General Medical Sciences","NIGMS NIH HHS"],"pagination":["RP88024"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11594533"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12"],"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"],"journal":["eLife"],"pubmed_title":["ARID1A governs the silencing of sex-linked transcription during male meiosis in the mouse."],"pmcid":["PMC11594533"],"funding_grant_id":["P30 CA016086","R01GM101974","R01 GM101974"],"pubmed_authors":["Magnuson T","Chakraborty P","Menon DU","Murcia N"],"additional_accession":[]},"is_claimable":false,"name":"ARID1A governs the silencing of sex-linked transcription during male meiosis in the mouse.","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","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-06-01T13:24:05.036Z","creation":"2025-04-04T22:47:50.913Z"},"accession":"S-EPMC11594533","cross_references":{"pubmed":["39589400"],"doi":["10.7554/eLife.88024"]}}