ArticleGenome research2016
Loss of HP1 causes depletion of H3K27me3 from facultative heterochromatin and gain of H3K27me2 at constitutive heterochromatin.
Article in Genome research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 120 citations in OpenAlex.
- Chromatin Assembly Factor 1 is required for normal structure and function of facultative heterochromatin inbioRxiv : the preprint server for biology · 2026Article
- Centromeres are hotspots of cytosine methylation epimutations in a filamentous fungus.bioRxiv : the preprint server for biology · 2026Article
- Article
- HISTONE DEACETYLASE-1 is required for epigenome stability inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Analysis of histone modification interplay reveals two distinct domains in facultative heterochromatin in Pyricularia oryzae.Communications biology · 2025Article
- Mapping the nuclear landscape with multiplexed super-resolution fluorescence microscopy.Nature communications · 2025Article
- RID is required for both repeat-induced point mutation and nucleation of a novel transitional heterochromatic state for euchromatic repeats.Nucleic acids research · 2025Article
- A constitutive heterochromatic region shapes genome organization and impacts gene expression in Neurospora crassa.BMC genomics · 2024Article
- A vector system encoding histone H3 mutants facilitates manipulations of the neuronal epigenome.Scientific reports · 2024Article
- A Constitutive Heterochromatic Region Shapes Genome Organization and Impacts Gene Expression inbioRxiv : the preprint server for biology · 2024Article
- Remodeling of perturbed chromatin can initiate de novo transcriptional and post-transcriptional silencing.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Extracellular Matrix Cues Regulate Mechanosensing and Mechanotransduction of Cancer Cells.Cells · 2024Review
- H3K27me3 is vital for fungal development and secondary metabolite gene silencing, and substitutes for the loss of H3K9me3 in the plant pathogen Fusarium proliferatum.PLoS genetics · 2024Article
- 3D models of fungal chromosomes to enhance visual integration of omics data.NAR genomics and bioinformatics · 2023Article
- Histone deacetylation and cytosine methylation compartmentalize heterochromatic regions in the genome organization ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- SHIELD: a platform for high-throughput screening of barrier-type DNA elements in human cells.Nature communications · 2023Article
- Nuclear genome organization in fungi: from gene folding to Rabl chromosomes.FEMS microbiology reviews · 2023Article
- Inactivation of MrSir2 in Monascus ruber Influenced the Developmental Process and the Production of Monascus Azaphilone Pigments.Applied biochemistry and biotechnology · 2022Article
- Epigenetic factor competition reshapes the EMT landscape.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Methylated lysine 27 on histone H3 (H3K27me) marks repressed "facultative heterochromatin," including developmentally regulated genes in plants and animals. The mechanisms responsible for localization of H3K27me are largely unknown, perhaps in part because of the complexity of epigenetic regulatory networks. We used a relatively simple model organism bearing both facultative and constitutive heterochromatin, Neurospora crassa, to explore possible interactions between elements of heterochromatin. In higher eukaryotes, reductions of H3K9me3 and DNA methylation in constitutive heterochromatin have been variously reported to cause redistribution of H3K27me3. In Neurospora, we found that elimination of any member of the DCDC H3K9 methylation complex caused massive changes in the distribution of H3K27me; regions of facultative heterochromatin lost H3K27me3, while regions that are normally marked by H3K9me3 became methylated at H3K27. Elimination of DNA methylation had no obvious effect on the distribution of H3K27me. Elimination of HP1, which "reads" H3K9me3, also caused major changes in the distribution of H3K27me, indicating that HP1 is important for normal localization of facultative heterochromatin. Because loss of HP1 caused redistribution of H3K27me2/3, but not H3K9me3, these normally nonoverlapping marks became superimposed. Indeed, mass spectrometry revealed substantial cohabitation of H3K9me3 and H3K27me2 on H3 molecules from an hpo strain. Loss of H3K27me machinery (e.g., the methyltransferase SET-7) did not impact constitutive heterochromatin but partially rescued the slow growth of the DCDC mutants, suggesting that the poor growth of these mutants is partly attributable to ectopic H3K27me. Altogether, our findings with Neurospora clarify interactions of facultative and constitutive heterochromatin in eukaryotes.
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