Histone acetyltransferase RTT109 required for epigenetic maintenance of PRC2-repressed chromatin in Neurospora
A PLOS Genetics study in the model fungus Neurospora crassa identifies RTT109 as a key regulator of Polycomb-silenced chromatin domains, acting independently of its canonical H3K56 acetylation activity.
Researchers including Rochelle E. Yap and colleagues have published findings in PLOS Genetics identifying the histone acetyltransferase RTT109 as a critical factor in maintaining chromatin domains repressed by Polycomb Repressive Complex 2 (PRC2) in the model fungus Neurospora crassa.
PRC2 establishes transcriptional silencing by catalysing trimethylation of histone H3 at lysine 27 (H3K27me3), a modification conserved across animals, plants, and some fungi. The study shows that RTT109 is required for the proper structure and function of these PRC2-methylated domains. Notably, the requirement is independent of H3K56 acetylation — the canonical substrate of RTT109 — indicating that the enzyme contributes to Polycomb silencing through a distinct, as-yet-uncharacterised mechanism. RTT109 was found to interact with the Vps75 homologue Nucleosome Assembly Factor 2 (NAF-2), though NAF-2 interaction alone does not account for the epigenetic maintenance function.
The work uses Neurospora as a tractable genetic system in which PRC2 biology can be dissected with fine resolution. The findings contribute to the broader question of how Polycomb-mediated gene silencing — implicated in development, differentiation, and cancer — is maintained through cell division, and raise the possibility that acetyltransferases play underappreciated roles in heterochromatin stability beyond their direct histone modification targets.
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Primary source Public Library of Science · 2026-10-05Epigenetic maintenance of PRC2-repressed chromatin requires RTT109 but not H3K56 acetylation