{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Garcia Fernandez F"],"funding":["Fondation ARC pour la Recherche sur le Cancer","Labex ‘Who am I?’","Agence Nationale de la Recherche","Université de Paris","National Institutes of Health","Fondation pour la Recherche Médicale","Consejo Nacional de Ciencia, Tecnología e Innovación Tecnológica","IDEX SLI","National Institute of General Medical Sciences","Cancéropôle Ile de France"],"pagination":["jcs258500"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8034873"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["134(6)"],"pubmed_abstract":["In budding yeast and mammals, double-strand breaks (DSBs) trigger global chromatin mobility together with rapid phosphorylation of histone H2A over an extensive region of the chromatin. To assess the role of H2A phosphorylation in this response to DNA damage, we have constructed strains where H2A has been mutated to the phosphomimetic H2A-S129E. We show that mimicking H2A phosphorylation leads to an increase in global chromatin mobility in the absence of DNA damage. The intrinsic chromatin mobility of H2A-S129E is not due to downstream checkpoint activation, histone degradation or kinetochore anchoring. Rather, the increased intrachromosomal distances observed in the H2A-S129E mutant are consistent with chromatin structural changes. Strikingly, in this context the Rad9-dependent checkpoint"],"journal":["Journal of cell science"],"pubmed_title":["Modified chromosome structure caused by phosphomimetic H2A modulates the DNA damage response by increasing chromatin mobility in yeast."],"pmcid":["PMC8034873"],"funding_grant_id":["DXCAIUHSLI-EF14","T32GM007122","ANR-18-IDEX-0001","DOC20190508798","ANR-13-BSV8-0013-01 ANR-11-IDEX-0005-02","ORFOCRISE PME-2015","R35 127029","ING20160435205","ANR-11-LABX-0071"],"pubmed_authors":["Batrin R","Garcia Fernandez F","Haber JE","Fabre E","Lemos B","Khalil Y"],"additional_accession":[]},"is_claimable":false,"name":"Modified chromosome structure caused by phosphomimetic H2A modulates the DNA damage response by increasing chromatin mobility in yeast.","description":"In budding yeast and mammals, double-strand breaks (DSBs) trigger global chromatin mobility together with rapid phosphorylation of histone H2A over an extensive region of the chromatin. To assess the role of H2A phosphorylation in this response to DNA damage, we have constructed strains where H2A has been mutated to the phosphomimetic H2A-S129E. We show that mimicking H2A phosphorylation leads to an increase in global chromatin mobility in the absence of DNA damage. The intrinsic chromatin mobility of H2A-S129E is not due to downstream checkpoint activation, histone degradation or kinetochore anchoring. Rather, the increased intrachromosomal distances observed in the H2A-S129E mutant are consistent with chromatin structural changes. Strikingly, in this context the Rad9-dependent checkpoint","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Mar","modification":"2025-04-29T11:31:35.084Z","creation":"2025-04-06T19:54:21.279Z"},"accession":"S-EPMC8034873","cross_references":{"pubmed":["33622771"],"doi":["10.1242/jcs.258500"]}}