{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Guo P"],"funding":["NIDDK NIH HHS","NIAID NIH HHS","NHLBI NIH HHS","European Hematology Association","NIH HHS","NIGMS NIH HHS"],"pagination":["99-111"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9166935"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(1)"],"pubmed_abstract":["Histone variants and the associated post-translational modifications that govern the stemness of haematopoietic stem cells (HSCs) and differentiation thereof into progenitors (HSPCs) have not been well defined. H3.3 is a replication-independent H3 histone variant in mammalian systems that is enriched at both H3K4me3- and H3K27me3-marked bivalent genes as well as H3K9me3-marked endogenous retroviral repeats. Here we show that H3.3, but not its chaperone Hira, prevents premature HSC exhaustion and differentiation into granulocyte-macrophage progenitors. H3.3-null HSPCs display reduced expression of stemness and lineage-specific genes with a predominant gain of H3K27me3 marks at their promoter regions. Concomitantly, loss of H3.3 leads to a reduction of H3K9me3 marks at endogenous retroviral "],"journal":["Nature cell biology"],"pubmed_title":["Histone variant H3.3 maintains adult haematopoietic stem cell homeostasis by enforcing chromatin adaptability."],"pmcid":["PMC9166935"],"funding_grant_id":["RM1 GM139738","R35 HL150809","R01 AI148416","U01 AI138329","TRTH153","R01 GM129380","R01 HL130826","R21 OD031973","RC2 DK114777"],"pubmed_authors":["Ding BS","Lis R","Xiang J","Tang F","Guo P","Daman AW","Liu X","Liu Y","Zhang T","Ravishankar A","Geng F","Barcia Duran JG","Itkin T","Shido K","Rafii S","Wen D","Zhong L","Josefowicz SZ"],"additional_accession":[]},"is_claimable":false,"name":"Histone variant H3.3 maintains adult haematopoietic stem cell homeostasis by enforcing chromatin adaptability.","description":"Histone variants and the associated post-translational modifications that govern the stemness of haematopoietic stem cells (HSCs) and differentiation thereof into progenitors (HSPCs) have not been well defined. H3.3 is a replication-independent H3 histone variant in mammalian systems that is enriched at both H3K4me3- and H3K27me3-marked bivalent genes as well as H3K9me3-marked endogenous retroviral repeats. Here we show that H3.3, but not its chaperone Hira, prevents premature HSC exhaustion and differentiation into granulocyte-macrophage progenitors. H3.3-null HSPCs display reduced expression of stemness and lineage-specific genes with a predominant gain of H3K27me3 marks at their promoter regions. Concomitantly, loss of H3.3 leads to a reduction of H3K9me3 marks at endogenous retroviral ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2026-06-03T10:18:33.531Z","creation":"2025-02-18T23:36:08.462Z"},"accession":"S-EPMC9166935","cross_references":{"pubmed":["34961794"],"doi":["10.1038/s41556-021-00795-7"]}}