ArticleGenes & development2012
Mechanism for epigenetic variegation of gene expression at yeast telomeric heterochromatin.
Article in Genes & development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 71 citations in OpenAlex.
- Regions of low gene expression promote maintenance and adaptation of horizontally acquired genes in yeasts.Communications biology · 2026Article
- Review
- Epigenetic state and gene expression remain stable after CRISPR/Cas-mediated chromosomal inversions.The New phytologist · 2025Article
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- Sir2 and Fun30 regulate ribosomal DNA replication timing via MCM helicase positioning and nucleosome occupancy.bioRxiv : the preprint server for biology · 2024Article
- Glc7/PP1 dephosphorylates histone H3T11 to regulate autophagy and telomere silencing in response to nutrient availability.Cell discovery · 2023Article
- Regulatory Roles of Histone Modifications in Filamentous Fungal Pathogens.Journal of fungi (Basel, Switzerland) · 2022Review
- Spreading-dependent or independent Sir2-mediated gene silencing in budding yeast.Genes & genomics · 2022Article
- Genome-nanosurface interaction of titania nanotube arrays: evaluation of telomere, telomerase and NF-κB activities on an epithelial cell model.RSC advances · 2022Article
- Article
- Ready, SET, Go: Post-translational regulation of the histone lysine methylation network in budding yeast.The Journal of biological chemistry · 2021Review
- Metabolic regulation of telomere silencing by SESAME complex-catalyzed H3T11 phosphorylation.Nature communications · 2021Article
- INO80C Remodeler Maintains Genomic Stability by Preventing Promiscuous Transcription at Replication Origins.Cell reports · 2020Article
- S-phase-independent silencing establishment ineLife · 2020Article
- Yeast mismatch repair components are required for stable inheritance of gene silencing.PLoS genetics · 2020Article
- Existence, Transition, and Propagation of Intermediate Silencing States in Ribosomal DNA.Molecular and cellular biology · 2019Article
- Yeast epigenetics: the inheritance of histone modification states.Bioscience reports · 2019Review
- A SIR-independent role for cohesin in subtelomeric silencing and organization.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Expanding heterochromatin reveals discrete subtelomeric domains delimited by chromatin landscape transitions.Genome research · 2018Article
- The interplay of histone H2B ubiquitination with budding and fission yeast heterochromatin.Current genetics · 2018Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Yeast contains heterochromatin at telomeres and the silent mating-type loci (HML/HMR). Genes positioned within the telomeric heterochromatin of Saccharomyces cerevisiae switch stochastically between epigenetically bistable ON and OFF expression states. Important aspects of the mechanism of variegated gene expression, including the chromatin structure of the natural ON state and the mechanism by which it is maintained, are unknown. To address this issue, we developed approaches to select cells in the ON and OFF states. We found by chromatin immunoprecipitation (ChIP) that natural ON telomeres are associated with Rap1 binding and, surprisingly, also contain known characteristics of OFF telomeres, including significant amounts of Sir3 and H4K16 deacetylated nucleosomes. Moreover, we found that H3K79 methylation (H3K79me), H3K4me, and H3K36me, which are depleted from OFF telomeres, are enriched at ON telomeres. We demonstrate in vitro that H3K79me, but not H3K4me or H3K36me, disrupts transcriptional silencing. Importantly, H3K79me does not significantly reduce Sir complex binding in vivo or in vitro. Finally, we show that maintenance of H3K79me at ON telomeres is dependent on transcription. Therefore, although Sir proteins are required for silencing, we propose that epigenetic variegation of telomeric gene expression is due to the bistable enrichment/depletion of H3K79me and not the fluctuation in the amount of Sir protein binding to nucleosomes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.