Integrated hypothetical model for post-translational modification (PTM)-dependent regulation of Polycomb Repressive Complex (PRC)1-mediated repression. Three independent chromatin states in the context of PRC1 function are recognized: (a) the repressed state, which requires ubiquitylation and sumoylation of PRC1 compounds. Detectable baseline phosphorylation may indicate a prerequisite for PRC function and/or differences in PRC activity at local targets throughout the genome. Signaling to chromatin alters PTM states and chromatin association, and eventually releases PRC silencing (b,c). Observations from our and other groups suggest differential regulation of polyhomeotic homolog (PHC) proteins versus RNF2, BMI1 and chromobox homolog (CBX) proteins; this may involve N-acetylglucosamine (GlcNAc) modification in mammals as well. (c) Whether or not full expression of a Polycomb Group (PcG) target gene requires complete removal or relocation of PHC is currently not known. Likewise, whether ubiquitin-mediated proteolysis of BMI1 and RNF2 is needed to release gene repression is purely speculative. ph = phosphorylation; su = sumoylation; ub = ubiquitylation. Black triangles = H3K27me3; open circles = H3S28ph; unmarked circular/oval structures represent general transcription factors and/or unknown proteins.