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The  INK4a/ARF  tumor suppressor locus, a key executor of cellular senescence, is regulated by members of the Polycomb group (PcG) of transcriptional repressors. Here we show that signaling from oncogenic RAS overrides PcG-mediated repression of  INK4a  by activating the H3K27 demethylase JMJD3 and down-regulating the methyltransferase EZH2. In human fibroblasts, JMJD3 activates  INK4a , but not  ARF , and causes p16 INK4a -dependent arrest. In mouse embryo fibroblasts, Jmjd3 activates both  Ink4a  and  Arf  and elicits a p53-dependent arrest, echoing the effects of RAS in this system. Our findings directly implicate JMJD3 in the regulation of  INK4a/ARF  during oncogene-induced senescence and suggest that JMJD3 has the capacity to act as a tumor suppressor.

Histone demethylase JMJD3 contributes to epigenetic control of INK4a/ARF by oncogenic RAS