{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Bjeije H"],"funding":["NIDDK NIH HHS","NHLBI NIH HHS","NCI NIH HHS"],"pubmed_abstract":["Previous studies showed the Polycomb Repressive Complex 2 (PRC2) co-factor Jarid2 represses self-renewal transcriptional networks in mouse multipotent progenitor cells (MPPs). But only a fraction of de-repressed HSC-specific genes were associated with loss of H3K27me3, implying Jarid2 may have non-canonical (PRC2-indpendent) in hematopoiesis. Here we sought to delineate any PRC2-independnent functions by comparing stem and progenitor cells genetically deficient for either <i>Jarid2</i> or <i>Ezh2</i> (enzymatic component of PRC2). Loss of <i>Ezh2</i> increased myeloid differentiation in transplantation assays. In contrast, loss of <i>Jarid2</i> enhanced T-cell output. Single cell transcriptomics showed while loss of <i>Jarid2</i> had minimal impact across progenitor populations, loss of <i"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2025.07.18.665536"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12338735"],"repository":["biostudies-literature"],"pubmed_title":["Functional Comparison to Ezh2 Reveals PRC2-Independent Functions of Jarid2 in Hematopoietic Stem Cell Lineage Commitment."],"pmcid":["PMC12338735"],"funding_grant_id":["R01 HL147978","P30 CA091842","R01 CA236819","R01 DK124883","R01 HL152180"],"pubmed_authors":["Raj IX","Challen GA","Yang W","Li Y","Magee JA","Arand J","Han W","Issa N","Bjeije H","Krishnan A"],"additional_accession":[]},"is_claimable":false,"name":"Functional Comparison to Ezh2 Reveals PRC2-Independent Functions of Jarid2 in Hematopoietic Stem Cell Lineage Commitment.","description":"Previous studies showed the Polycomb Repressive Complex 2 (PRC2) co-factor Jarid2 represses self-renewal transcriptional networks in mouse multipotent progenitor cells (MPPs). But only a fraction of de-repressed HSC-specific genes were associated with loss of H3K27me3, implying Jarid2 may have non-canonical (PRC2-indpendent) in hematopoiesis. Here we sought to delineate any PRC2-independnent functions by comparing stem and progenitor cells genetically deficient for either <i>Jarid2</i> or <i>Ezh2</i> (enzymatic component of PRC2). Loss of <i>Ezh2</i> increased myeloid differentiation in transplantation assays. In contrast, loss of <i>Jarid2</i> enhanced T-cell output. Single cell transcriptomics showed while loss of <i>Jarid2</i> had minimal impact across progenitor populations, loss of <i","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jul","modification":"2026-04-08T03:50:12.774Z","creation":"2026-04-07T21:41:37.966Z"},"accession":"S-EPMC12338735","cross_references":{"pubmed":["40791535"],"doi":["10.1101/2025.07.18.665536"]}}