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. 2022 Dec 2;6(4):42. doi: 10.3390/epigenomes6040042

Figure 2.

Figure 2

Schematic representation of Polycomb group (PcG) protein recruitment and chromatin binding. The PRC family is targeted to chromatin by a hierarchical process. Initial localisation occurs through sequence specific and/or direct recruitment mechanisms that in turn lead to the deposition of chromatin modifications that act to recruit or activate downstream PRCs. Transcriptionally silent, non-methylated CpG islands (CGIs), provide a direct recruitment platform for both PRC2.1 and PRC1.1 via affinity of their Polycomb-like (PCL; PCL1-3) and Lysine Demethylase 2B (KDM2B) subunits respectively [10,19,63,64,65,66]. In addition, other ncPRCs employ both sequence specific and RNA-mediated mechanisms to target specific sites in the genome (the varying subunits responsible for chromatin targeting of individual ncPRC1s, including KDM2B, are denoted as X for simplicity) [67,68,69,70,71,72]. This leads to the deposition of H3K27me3 by EZH1/2 (PRC2.1) and H2AK119ub1 by RING1A/B (ncPRC1). The resulting H2A ubiquitination leads to the recruitment and allosteric activation of PRC2.2, through association with JARID2 and AEBP2, which enhances H3K27me3 deposition [12,73,74,75]. Finally, cPRC1 is recruited to chromatin by CBX7-mediated recognition of PRC2-deposited H3K27me3, where it nucleates physical interactions between other cPRC1 target sites in the genome [22,29,31,37,38,42]. However, due to its very low E3 ubiquitin ligase activity, cPRC1 contributes little to the deposition of H2AK119ub1 (denoted by a faint dashed arrow), which is primarily carried out by ncPRC1s [54,55].