Direct recruitment of polycomb repressive complex 1 to chromatin by core binding transcription factors
- Authors
- Yu, M., Mazor, T., Huang, H., Huang, H.T., Kathrein, K.L., Woo, A.J., Chouinard, C.R., Labadorf, A., Akie, T.E., Moran, T.B., Xie, H., Zacharek, S., Taniuchi, I., Roeder, R.G., Kim, C.F., Zon, L.I., Fraenkel, E., and Cantor, A.B.
- ID
- ZDB-PUB-120730-16
- Date
- 2012
- Source
- Molecular Cell 45(3): 330-343 (Journal)
- Registered Authors
- Zon, Leonard I.
- Keywords
- none
- MeSH Terms
-
- Polycomb-Group Proteins
- Mice, Knockout
- Cell Line
- Proto-Oncogene Proteins/genetics
- Proto-Oncogene Proteins/metabolism
- Gene Expression Regulation
- Animals
- Mice
- Chromatin/metabolism*
- Cluster Analysis
- Hematopoietic Stem Cells/physiology
- Core Binding Factor Alpha 2 Subunit/genetics
- Core Binding Factor Alpha 2 Subunit/metabolism*
- Protein Multimerization
- Gene Knockdown Techniques
- T-Lymphocytes/metabolism
- Thymocytes/metabolism
- Zebrafish/embryology
- Zebrafish/genetics
- Core Binding Factor beta Subunit/genetics
- Core Binding Factor beta Subunit/metabolism*
- Chromatography, Affinity
- Mice, Inbred C57BL
- Nuclear Proteins/genetics
- Nuclear Proteins/metabolism
- Megakaryocytes/metabolism
- Repressor Proteins/genetics
- Repressor Proteins/isolation & purification
- Repressor Proteins/metabolism*
- Protein Binding
- Gene Expression Profiling
- Ubiquitin-Protein Ligases/genetics
- Ubiquitin-Protein Ligases/metabolism
- Polycomb Repressive Complex 1
- PubMed
- 22325351 Full text @ Mol. Cell
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/CBFβ transcription factor complex. Genome-wide studies in megakaryocytic cells demonstrate significant chromatin occupancy overlap between the PRC1 core component Ring1b and Runx1/CBFβ and functional regulation of a considerable fraction of commonly bound genes. Bmi1/Ring1b and Runx1/CBFβ 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.