Chromatin Assembly Factor 1 required for normal facultative heterochromatin in Neurospora crassa, preprint finds
A bioRxiv preprint demonstrates that loss of the replication-coupled histone chaperone CAF-1 disrupts PRC2-directed H3K27me3 heterochromatin structure and causes widespread transcriptional misregulation in the model fungus Neurospora crassa.
A preprint posted to bioRxiv on 16 June 2026 describes a functional role for Chromatin Assembly Factor 1 (CAF-1) in maintaining the structure and transcriptional silencing activity of facultative heterochromatin in the filamentous fungus Neurospora crassa.
Facultative heterochromatin — genomic regions silenced in a developmentally regulated, rather than constitutive, manner — is established and maintained in many eukaryotes by Polycomb Repressive Complex 2 (PRC2), which methylates histone H3 at lysine 27 (H3K27me3). CAF-1 is a replication-dependent histone chaperone that deposits histones H3 and H4 during DNA synthesis. The authors report that loss of CAF-1 in Neurospora causes widespread transcriptional misregulation, with particular effects on genes normally silenced by PRC2-mediated facultative heterochromatin, suggesting that replication-coupled histone deposition is required to propagate H3K27me3 chromatin domains through cell division.
Neurospora crassa is an established model organism for studying epigenetic regulation, including both constitutive and facultative heterochromatin. The finding adds to a growing body of evidence that the machinery linking DNA replication to chromatin re-establishment is critical for maintaining epigenetic gene-silencing programmes. This preprint has not yet undergone formal peer review.
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Primary sourcePreprint bioRxiv (Cold Spring Harbor Laboratory) · 2026-06-16Chromatin Assembly Factor 1 is required for normal structure and function of facultative heterochromatin in Neurospora crassa