Journal
GENES & DEVELOPMENT
Volume 21, Issue 1, Pages 49-54Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1499407
Keywords
p16; pRB; BMI1; PRC1; PRC2; transcriptional regulation
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Funding
- NCI NIH HHS [CA68377, R01 CA068377] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA068377] Funding Source: NIH RePORTER
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Genetic studies have demonstrated that Bmi1 promotes cell proliferation and stem cell self-renewal with a correlative decrease of p16(INK4a) expression. Here, we demonstrate that Polycomb genes EZH2 and BMI1 repress p16 expression in human and mouse primary cells, but not in cells deficient for pRB protein function. The p16 locus is H3K27-methylated and bound by BMI1, RING2, and SUZ12. Inactivation of pRB family proteins abolishes H3K27 methylation and disrupts BMI1, RING2, and SUZ12 binding to the p16 locus. These results suggest a model in which pRB proteins recruit PRC2 to trimethylate p16, priming the BMI1-containing PRC1L ubiquitin ligase complex to silence p16.
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