期刊
SCIENCE ADVANCES
卷 6, 期 32, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.abb2745
关键词
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资金
- Spanish of Economy, Industry, and Competitiveness (MEIC) [BFU2016-75008-P]
- Fundacion Vencer El Cancer (VEC)
- European Regional Development Fund (FEDER)
- Fundacio La Marato de TV3
- AGAUR
- Ministerio de Ciencia, Innovacion y Universidades [SAF2016-75613-R]
- Spanish Institute of Health Carlos III (ISCIII) [CP14/00229]
- European Union's Horizon 2020 research and innovation programme [MSCA-ITN-2015-675752]
- Ministerio de Ciencia, Innovacion y Universidades (AEI/FEDER, UE) [SAF2017-89109-P]
- Fundacion Cientifica de la Asociacion Espanola Contra el Cancer
- La Caixa INPhINIT program
- FPI Program
- Generalitat de Catalunya (Beatriu de Pinos program) [2016 BP 00021]
- Spanish MEIC through the Instituto de Salud Carlos III
- EMBL partnership
- Centro de Excelencia Severo Ochoa
- CERCA Programme/Generalitat de Catalunya
- Generalitat de Catalunya through Departament de Salut
- Departament d'Empresa i Coneixement
- Spanish Ministry of Economy, Industry and Competitiveness (MEIC)
- European Regional Development Fund (ERDF)
Adult hematopoietic stem cells (HSCs) are rare multipotent cells in bone marrow that are responsible for generating all blood cell types. HSCs are a heterogeneous group of cells with high plasticity, in part, conferred by epigenetic mechanisms. PHF19, a subunit of the Polycomb repressive complex 2 (PRC2), is preferentially expressed in mouse hematopoietic precursors. Here, we now show that, in stark contrast to results published for other PRC2 subunits, genetic depletion of Phf19 increases HSC identity and quiescence. While proliferation of HSCs is normally triggered by forced mobilization, defects in differentiation impede long-term correct blood production, eventually leading to aberrant hematopoiesis. At molecular level, PHF19 deletion triggers a redistribution of the histone repressive mark H3K27me3, which notably accumulates at blood lineage-specific genes. Our results provide novel insights into how epigenetic mechanisms determine HSC identity, control differentiation, and are key for proper hematopoiesis.
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