Journal
SCIENCE
Volume 351, Issue 6274, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aad5510
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Funding
- European Union
- La Fondation de France
- La Ligue Nationale Contre le Cancer (Equipe Labelisee)
- Human Frontier Science Program long-term fellowship
- Stiftung Charite
- Fondation ARC pour la Recherche sur le Cancer
- Fondation pour la Recherche Medicale [AJE20130728183, DEQ20110421320]
- NIH National Institute on Aging [P01AG036695]
- Agence Nationale de la Recherche [ANR-11-BSV3-026-01]
- Institut National du Cancer [13-10/405/AB-LC-HS]
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Differentiated macrophages can self-renew in tissues and expand long term in culture, but the gene regulatory mechanisms that accomplish self-renewal in the differentiated state have remained unknown. Here we show that in mice, the transcription factors MafB and c-Maf repress a macrophage-specific enhancer repertoire associated with a gene network that controls self-renewal. Single-cell analysis revealed that, in vivo, proliferating resident macrophages can access this network by transient down-regulation of Maf transcription factors. The network also controls embryonic stem cell self-renewal but is associated with distinct embryonic stem cell-specific enhancers. This indicates that distinct lineage-specific enhancer platforms regulate a shared network of genes that control self-renewal potential in both stem and mature cells.
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