ArticleNucleic acids research2022
H3K56 deacetylation and H2A.Z deposition are required for aberrant heterochromatin spreading.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Isomucronulatol attenuates liver aging by inhibiting GSK-3β acetylation and promoting β-catenin accumulation.Journal of natural medicines · 2026Article
- H2A.Z-nucleosomes are stabilized by the superhelicity-dependent DNA binding of the C-terminal tail of the histone variant.Nucleus (Austin, Tex.) · 2025Article
- Restoration of SIRT3 Expression in Aged Mice Alleviates UUO-Induced Renal Fibrosis by Reducing GSK-3β Hyperacetylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Checkpoint kinases regulate the circadian clock after DNA damage by influencing chromatin dynamics.Nucleic acids research · 2025Article
- H3T11 phosphorylation by CKII is required for heterochromatin formation in Neurospora.Nucleic acids research · 2024Article
- Incorporation of the histone variant H2A.Z counteracts gene silencing mediated by H3K27 trimethylation in Fusarium fujikuroi.Epigenetics & chromatin · 2024Article
- Coevolution of the CDCA7-HELLS ICF-related nucleosome remodeling complex and DNA methyltransferases.eLife · 2023Article
- Coevolution of the CDCA7-HELLS ICF-related nucleosome remodeling complex and DNA methyltransferases.bioRxiv : the preprint server for biology · 2023Article
- Functional analysis of 110 phosphorylation sites on the circadian clock protein FRQ identifies clusters determining period length and temperature compensation.G3 (Bethesda, Md.) · 2023Article
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Crucial mechanisms are required to restrict self-propagating heterochromatin spreading within defined boundaries and prevent euchromatic gene silencing. In the filamentous fungus Neurospora crassa, the JmjC domain protein DNA METHYLATION MODULATOR-1 (DMM-1) prevents aberrant spreading of heterochromatin, but the molecular details remain unknown. Here, we revealed that DMM-1 is highly enriched in a well-defined 5-kb heterochromatin domain upstream of the cat-3 gene, hereby called 5H-cat-3 domain, to constrain aberrant heterochromatin spreading. Interestingly, aberrant spreading of the 5H-cat-3 domain observed in the dmm-1KO strain is accompanied by robust deposition of histone variant H2A.Z, and deletion of H2A.Z abolishes aberrant spreading of the 5H-cat-3 domain into adjacent euchromatin. Furthermore, lysine 56 of histone H3 is deacetylated at the expanded heterochromatin regions, and mimicking H3K56 acetylation with an H3K56Q mutation effectively blocks H2A.Z-mediated aberrant spreading of the 5H-cat-3 domain. Importantly, genome-wide analyses demonstrated the general roles of H3K56 deacetylation and H2A.Z deposition in aberrant spreading of heterochromatin. Together, our results illustrate a previously unappreciated regulatory process that mediates aberrant heterochromatin spreading.
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