ArticleNucleic acids research2025
RID is required for both repeat-induced point mutation and nucleation of a novel transitional heterochromatic state for euchromatic repeats.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- 5mC and 6mA DNA Methylation in the Fungal Kingdom: From Genome Defense to Epigenetic Regulation.Epigenomes · 2026Review
- Epigenetic Inhibitor 5-Azacytidine Triggers DIM-2/DIM-5-Dependent Mutagenesis in H3K9me3-Enriched Regions ofJournal of fungi (Basel, Switzerland) · 2026Article
- Centromeres are hotspots of cytosine methylation epimutations in a filamentous fungus.bioRxiv : the preprint server for biology · 2026Article
- Phylogenomic signatures of repeat-induced point mutations across the fungal kingdom.PLoS biology · 2025Article
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Authors and funding
12 authors.
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Abstract
To maintain genome integrity, repeat sequences are subject to heterochromatin inactivation and, in Neurospora, repeat-induced point mutation (RIP). The initiating factors behind both are poorly understood. We resolve the paradoxical observation that newly introduced Repeat-Linker-Repeat (R-L-R) constructs require RID alone for RIP, while genomic repeats are RIPed in the absence of RID, showing that eu- and hetero- chromatic repeats are handled differently, the latter additionally requiring DIM-2. The differences between mechanisms associated with older and newer duplicates caution against extrapolation from mechanisms inferred from model experimental systems. Additionally, while chromatin status affects RIP, we also show that RID, when tethered with LexA, acts as a nucleation center for the transition from euchromatin to heterochromatin in an HDA-1 dependent fashion. Constitutive heterochromatin by contrast is largely HDA1 independent and depends on HDA-1 paralogs. RID is thus a dual function initiator of both RIP and the transition to heterochromatin.
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