{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bomber ML"],"funding":["NCATS NIH HHS","NCRR NIH HHS","NIDDK NIH HHS","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["507-522.e6"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9974918"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["83(4)"],"pubmed_abstract":["Genetic models suggested that SMARCA5 was required for DNA-templated events including transcription, DNA replication, and DNA repair. We engineered a degron tag into the endogenous alleles of SMARCA5, a catalytic component of the imitation switch complexes in three different human cell lines to define the effects of rapid degradation of this key regulator. Degradation of SMARCA5 was associated with a rapid increase in global nucleosome repeat length, which may allow greater chromatin compaction. However, there were few changes in nascent transcription within the first 6 h of degradation. Nevertheless, we demonstrated a requirement for SMARCA5 to control nucleosome repeat length at G<sub>1</sub>/S and during the S phase. SMARCA5 co-localized with CTCF and H2A.Z, and we found a rapid loss of"],"journal":["Molecular cell"],"pubmed_title":["Human SMARCA5 is continuously required to maintain nucleosome spacing."],"pmcid":["PMC9974918"],"funding_grant_id":["R01 CA164605","R01 CA255446","F32 CA174162","R35 GM147213","UL1 RR024975","P30 CA068485","P30 DK058404","T32 CA009582","UL1 TR000445"],"pubmed_authors":["Hodges E","Layden HM","Liu Q","Stengel KR","Bomber ML","Hiebert SW","Wang J","Barnett KR"],"additional_accession":[]},"is_claimable":false,"name":"Human SMARCA5 is continuously required to maintain nucleosome spacing.","description":"Genetic models suggested that SMARCA5 was required for DNA-templated events including transcription, DNA replication, and DNA repair. We engineered a degron tag into the endogenous alleles of SMARCA5, a catalytic component of the imitation switch complexes in three different human cell lines to define the effects of rapid degradation of this key regulator. Degradation of SMARCA5 was associated with a rapid increase in global nucleosome repeat length, which may allow greater chromatin compaction. However, there were few changes in nascent transcription within the first 6 h of degradation. Nevertheless, we demonstrated a requirement for SMARCA5 to control nucleosome repeat length at G<sub>1</sub>/S and during the S phase. SMARCA5 co-localized with CTCF and H2A.Z, and we found a rapid loss of","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2026-05-28T21:55:07.404Z","creation":"2025-02-18T23:23:54.464Z"},"accession":"S-EPMC9974918","cross_references":{"pubmed":["36630954"],"doi":["10.1016/j.molcel.2022.12.018"]}}