{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shankar A"],"funding":["European Hematology Association (EHA)","Kay Kendall Leukaemia Fund","Leukemia and Lymphoma Society (Leukemia & Lymphoma Society)","European Hematology Association","Kay Kendall Leukaemia Fund (KKLF)","U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute","Wellcome Trust","U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI)","Leukemia and Lymphoma Society"],"pagination":["1756"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12914052"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(1)"],"pubmed_abstract":["The biological mechanisms that sustain the vast blood production required for healthy life remain incompletely understood. To search for cell intrinsic regulators of hematopoiesis, we perform a genome-wide in vivo hematopoietic stem and progenitor cell (HSPC)-based CRISPR knockout screen. We discover SAGA complex members, including Tada2b and Taf5l, as key regulators of hematopoiesis. Loss of Tada2b or Taf5l strongly inhibits hematopoiesis in vivo, causing a buildup of immature hematopoietic cells in the bone marrow. The SAGA complex deposits histone H3 lysine 9 acetylation (H3K9ac) and removes histone H2B ubiquitination (H2Bub). Loss of Tada2b leads to a reduction in H3K9ac levels and altered H2Bub enrichment in HSPCs, implicating disruption of SAGA complex activity. This is associated wi"],"journal":["Nature communications"],"pubmed_title":["In vivo CRISPR screening identifies SAGA complex members as key regulators of hematopoiesis."],"pmcid":["PMC12914052"],"funding_grant_id":["203151/A/16/Z","302479/Z/23/Z","K99HL150218","3385-19","KKL1378","302479Z23Z","RG-202211-02958"],"pubmed_authors":["Igarashi KJ","Meaker GA","Iwama A","Olender L","Palovics R","Wyss-Coray T","Haney MS","Wilkinson AC","Khoo HM","Rizq O","Nakauchi H","Mack PK","Shankar A","Kaito S","Tan TK","Bozhilov Y","Bhadury J","Miyauchi M","Munson C","Hsu I","Rehwinkel J"],"additional_accession":[]},"is_claimable":false,"name":"In vivo CRISPR screening identifies SAGA complex members as key regulators of hematopoiesis.","description":"The biological mechanisms that sustain the vast blood production required for healthy life remain incompletely understood. To search for cell intrinsic regulators of hematopoiesis, we perform a genome-wide in vivo hematopoietic stem and progenitor cell (HSPC)-based CRISPR knockout screen. We discover SAGA complex members, including Tada2b and Taf5l, as key regulators of hematopoiesis. Loss of Tada2b or Taf5l strongly inhibits hematopoiesis in vivo, causing a buildup of immature hematopoietic cells in the bone marrow. The SAGA complex deposits histone H3 lysine 9 acetylation (H3K9ac) and removes histone H2B ubiquitination (H2Bub). Loss of Tada2b leads to a reduction in H3K9ac levels and altered H2Bub enrichment in HSPCs, implicating disruption of SAGA complex activity. This is associated wi","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-07-16T06:56:45.392Z","creation":"2026-07-09T13:10:47.232Z"},"accession":"S-EPMC12914052","cross_references":{"pubmed":["41577693"],"doi":["10.1038/s41467-026-68465-6"]}}