ArticleEpigenetics2015
Cooperative stabilization of the SIR complex provides robust epigenetic memory in a model of SIR silencing in Saccharomyces cerevisiae.
Article in Epigenetics, 2015. 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, 19 citations in OpenAlex.
- Transcriptional silencing in Saccharomyces cerevisiae: known unknowns.Epigenetics & chromatin · 2024Review
- Two-way feedback between chromatin compaction and histone modification state explainsProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Yeast Heterochromatin Only Stably Silences Weak Regulatory Elements by Altering Burst Duration.bioRxiv : the preprint server for biology · 2023Article
- Two-way feedback between chromatin compaction and histone modification state explainsbioRxiv : the preprint server for biology · 2023Article
- Measuring the buffering capacity of gene silencing inProceedings of the National Academy of Sciences of the United States of America · 2021Article
- A programmable fate decision landscape underlies single-cell aging in yeast.Science (New York, N.Y.) · 2020Article
- Yeast epigenetics: the inheritance of histone modification states.Bioscience reports · 2019Review
- Epigenomics in 3D: importance of long-range spreading and specific interactions in epigenomic maintenance.Nucleic acids research · 2018Article
- Mixed-Lineage Leukemia Fusions and Chromatin in Leukemia.Cold Spring Harbor perspectives in medicine · 2017Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
How alternative chromatin-based regulatory states can be made stable and heritable in order to provide robust epigenetic memory is poorly understood. Here, we develop a stochastic model of the silencing system in Saccharomyces cerevisiae that incorporates cooperative binding of the repressive SIR complex and antisilencing histone modifications, in addition to positive feedback in Sir2 recruitment. The model was able to reproduce key features of SIR regulation of an HM locus, including heritable bistability, dependence on the silencer elements, and sensitivity to SIR dosage. We found that antisilencing methylation of H3K79 by Dot1 was not needed to generate these features, but acted to reduce spreading of SIR binding, consistent with its proposed role in containment of silencing. In contrast, cooperative inter-nucleosome interactions mediated by the SIR complex were critical for concentrating SIR binding around the silencers in the absence of barriers, and for providing bistability in SIR binding. SIR-SIR interactions magnify the cooperativity in the Sir2-histone deacetylation positive feedback reaction and complete a double-negative feedback circuit involving antisilencing modifications. Thus, our modeling underscores the potential importance of cooperative interactions between nucleosome-bound complexes both in the SIR system and in other chromatin-based complexes in epigenetic regulation.
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Registered trials
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.