ArticleDevelopmental cell2024
Mapping the dynamics of epigenetic adaptation in S. pombe during heterochromatin misregulation.
Article in Developmental cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Newly synthesized histones: passive or active players in the regulation of epigenetic inheritance?Nucleic acids research · 2026Review
- Neofunctionalization of H1 linker histones drives divergent gene expression and histone methylation in Cryptococcus neoformans.Communications biology · 2026Article
- An H3K14ub-H3K9me3 feedback circuit governs heterochromatin spreading and inheritance in fission yeast.Nature communications · 2026Article
- Heterochromatin epimutations impose mitochondrial dysfunction to confer antifungal resistance.The EMBO journal · 2026Article
- Noise-driven morphogenesis independent of transcriptional regulatory programs.bioRxiv : the preprint server for biology · 2025Article
- Loss ofmicroPublication biology · 2025Article
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Authors and funding
9 authors.
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Abstract
Epigenetic mechanisms enable cells to develop novel adaptive phenotypes without altering their genetic blueprint. Recent studies show histone modifications, such as heterochromatin-defining H3K9 methylation (H3K9me), can be redistributed to establish adaptive phenotypes. We developed a precision-engineered genetic approach to trigger heterochromatin misregulation on-demand in fission yeast. This enabled us to trace genome-scale RNA and H3K9me changes over time in long-term, continuous cultures. Adaptive H3K9me establishes over remarkably slow timescales relative to the initiating stress. We captured dynamic H3K9me redistribution events which depend on an RNA binding complex MTREC, ultimately leading to cells converging on an optimal adaptive solution. Upon stress removal, cells relax to new transcriptional and chromatin states, establishing memory that is tunable and primed for future adaptive epigenetic responses. Collectively, we identify the slow kinetics of epigenetic adaptation that allow cells to discover and heritably encode novel adaptive solutions, with implications for drug resistance and response to infection.
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