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Fig. 1 | Clinical Epigenetics

Fig. 1

From: Polycomb repressive complex’s evolutionary conserved function: the role of EZH2 status and cellular background

Fig. 1

Association of PRC-EZH2 complexes with different EED isoforms in the presence (H1+) or absence (H1−) of linker histone H1 directs EZH2-mediated methylation towards H3K27 or H1K26. PRC2, which contains the longest form of EED (EED1), is able to methylate isolated histone H3. When targeted to oligonucleosomes containing linker histone H1, PRC2 methylates histone H1 rather than histone H3. PRC3, containing EED3 and EED4, methylates nucleosomal histone H3, but its methyltransferase activity is inhibited by histone H1. PRC4, containing EED2 and NAD-dependent deacetylase SIRT1, methylates histone H1 when present, but has also low methylating capacity towards H3K27 in the absence of histone H1 (depicted in gray) [13, 14]

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