{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cenik BK"],"funding":["NICHD NIH HHS","NCI NIH HHS","National Institutes of Health","NIH HHS","NIGMS NIH HHS"],"pagination":["e2118385119"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9171609"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["119(19)"],"pubmed_abstract":["Embryonic stem cells (ESCs) are defined by their ability to self-renew and the potential to differentiate into all tissues of the developing organism. We previously demonstrated that deleting the catalytic SET domain of the Set1A/complex of proteins associated with SET1 histone methyltransferase (Set1A/COMPASS) in mouse ESCs does not impair their viability or ability to self-renew; however, it leads to defects in differentiation. The precise mechanisms by which Set1A executes these functions remain to be elucidated. In this study, we demonstrate that mice lacking the SET domain of Set1A are embryonic lethal at a stage that is unique from null alleles. To gain insight into Set1A function in regulating pluripotency, we conducted a CRISPR/Cas9-mediated dropout screen and identified the MOZ/MO"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["A synthetic lethality screen reveals ING5 as a genetic dependency of catalytically dead Set1A/COMPASS in mouse embryonic stem cells."],"pmcid":["PMC9171609"],"funding_grant_id":["R00 HD094906","S10 OD025194","R35 CA197569","K99 HD094906","R35CA197569","P30 CA060553","F99 CA234945","P41 GM108569"],"pubmed_authors":["Douillet D","Cao K","Shilatifard A","Zha D","Rendleman EJ","Khan NH","Sze CC","Das S","Ryan CA","Cenik BK","Bartom E"],"additional_accession":[]},"is_claimable":false,"name":"A synthetic lethality screen reveals ING5 as a genetic dependency of catalytically dead Set1A/COMPASS in mouse embryonic stem cells.","description":"Embryonic stem cells (ESCs) are defined by their ability to self-renew and the potential to differentiate into all tissues of the developing organism. We previously demonstrated that deleting the catalytic SET domain of the Set1A/complex of proteins associated with SET1 histone methyltransferase (Set1A/COMPASS) in mouse ESCs does not impair their viability or ability to self-renew; however, it leads to defects in differentiation. The precise mechanisms by which Set1A executes these functions remain to be elucidated. In this study, we demonstrate that mice lacking the SET domain of Set1A are embryonic lethal at a stage that is unique from null alleles. To gain insight into Set1A function in regulating pluripotency, we conducted a CRISPR/Cas9-mediated dropout screen and identified the MOZ/MO","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 May","modification":"2026-06-04T04:54:14.933Z","creation":"2025-04-05T11:27:38.687Z"},"accession":"S-EPMC9171609","cross_references":{"pubmed":["35500115"],"doi":["10.1073/pnas.2118385119"]}}