Fig. 7: Model for the role of R-loop formation driven by PRC2 in PcG gene silencing.
From: RNA-DNA strand exchange by the Drosophila Polycomb complex PRC2
Top panels (a, b) summarize our in vitro results with PRC2 (a, b) and PRC1 (b). Bottom panels (c, d) are a speculative model for how these activities could contribute to establishing or maintaining the OFF state at PREs. The ability of RNA to compete for PRC2 binding to chromatin is based on extensive observations in the literature. a PRC2 mediates RNA–DNA strand exchange, creating RNA–DNA hybrids. b PRC1 and PRC2 recognize R-loops. c Low levels of transcription through PREs could allow R-loop formation, which could depend on PRC2 activity (but could also be independent). R-loop formation sequesters the RNA and inhibits new RNA production, allowing PRC2 to be retained on chromatin. Recruitment of PRC1 and PRC2 (and other factors) may occur through recognition of the R-loop. d RNA produced by high levels of transcription competes for PRC2 binding to chromatin. See Discussion for details. This model is inspired by that of Ringrose12, but incorporates our new in vitro observations.
