Journal
MOLECULAR CELL
Volume 45, Issue 3, Pages 330-343Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2011.11.032
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Funding
- Wendy Will Case Cancer Fund
- American Heart Association
- NIH [R01-HL082952, U54-CA112967, R01-GM089903, P30-ES002109]
- Eugene Bell Career Development Chair
- National Science Foundation [DB1-0821391]
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Polycomb repressive complexes (PRCs) play key roles in developmental epigenetic regulation. Yet the mechanisms that target PRCs to specific loci in mammalian cells remain incompletely understood. In this study we show that Bmi1, a core component of Polycomb Repressive Complex 1 (PRC1), binds directly to the Runx1/CBF beta transcription factor complex. Genome-wide studies in megakaryocytic cells demonstrate significant chromatin occupancy overlap between the PRC1 core component Ring1b and Runx1/CBF beta and functional regulation of a considerable fraction of commonly bound genes. Bmi1/Ring1b and Runx1/CBF beta deficiencies generate partial phenocopies of one another in vivo. We also show that Ring1b occupies key Runx1 binding sites in primary murine thymocytes and that this occurs via PRC2-independent mechanisms. Genetic depletion of Runx1 results in reduced Ring1b binding at these sites in vivo. These findings provide evidence for site-specific PRC1 chromatin recruitment by core binding transcription factors in mammalian cells.
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