Figure 2.

Genome-wide Landscapes of PRC1 in TACs

(A) ChIP-seq on Ring1b, H3K4me3, and H3K27me3 identified 3,939, 14,361, and 11,341 gene loci, respectively. There were 2,624 gene loci co-occupied by both H3K4me3 and Ring1b, whereas 1,591 loci were marked with H3K27me3 and Ring1b.

(B) Genome browser snapshots representing repressive and active gene loci regulated by Ring1b.

(C) BigWIG metrics identified five clusters across targets in H3K4me3 and H3K27me3 active regions.

(D) Snapshots of genome browser showed the enrichment of PRC1 components in TACs.

(E and F) Double immunolocalization of Ki67 (E) with Cbx2 and Ring1b (F), respectively, in the TAC region.

(G) Flow-sorted EdU⁺ fast-cycling cells were collected by cytospin and immunofluorescence staining showed co-localization of Ring1b and Cbx2 on EdU⁺ cells.

(H) Co-immunoprecipitation with H2AK119ub1 and H3K27me27 on primary dental pulp cells by Ring1b antibody identified interaction of Ring1b and H3K27m3 rather than H2AK119ub1.

(I) Conditional knock out of Ring1b caused decreased levels of H3K27me3 demonstrated by western blots. Lamin B antibody was used as an internal loading control.

N ≥ 5 mice per group.