What is strongly supported: PRC2/EZH1/2 writes H3K27me3 and Polycomb systems maintain developmental repression; SUV39H/SETDB1-dependent H3K9me3 recruits HP1 and supports heterochromatin.
What is context-dependent: H3K27me3 bivalency can coexist with H3K4me3; H3K9me3 effects depend on repeats, lamina, and cell type.
What is weak, controversial, or assay-biased: Combining H3K27me3 and H3K9me3 is useful for a map but hides distinct readers, genomic targets, and dynamics.
What may be duplicate biology under another name: Overlaps with SILENCER and ZONES.
Missing or excessive graph structure
Missing edges: Add WRITER-R -> SILENCER reciprocal logic already present; could add WRITER-R -> FENCES/ZONES via heterochromatin compaction as context.
Excess edges: WRITER-R -> KEYS as compact chromatin exclusion is broadly true but should mention pioneer factors can bind some closed chromatin.
Candidate splits: Optional split Polycomb vs H3K9/HP1 heterochromatin in a detailed version.
Candidate merges: No merge.
Candidate renames: REPRESSIVE-HISTONE-MARKS.
Recommendation
Concrete graph change, if any: Keep; notes should distinguish Polycomb and H3K9 systems and pioneer-factor exceptions.
Concrete technical-notes/blog wording change, if any: Mirror the graph recommendation in the glossary and relation catalogue, and explicitly mark the confidence/caveat where the claim is context-dependent or assay-sensitive.
Key sources
PMID 31819266 — review of Polycomb repression mechanisms.