“…One possibility is that H2AK119ub1 directly disrupts RNA Pol II activity (Stock et al, 2007;Zhou et al, 2008), as suggested by in vitro transcription assays (Aihara et al, 2016;Nakagawa et al, 2008). Alternatively, H2AK119ub1 could recruit reader proteins that elicit gene repression (Ali et al, 2018;Cooper et al, 2016;Qin et al, 2015;Richly et al, 2010;Zhang et al, 2017) or interfere with deposition of histone modifications that facilitate transcription (Nakagawa et al, 2008;Yuan et al, 2013). Finally, it is possible that PRC1 drives gene repression via ubiquitylation of histone H2A variants (Surface et al, 2016) or other non-histone substrates (Ben-Saadon et al, 2006).…”