ArticleBiophysical journal2021
Impact of chromosomal organization on epigenetic drift and domain stability revealed by physics-based simulations.
Article in Biophysical journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- From linear methylation to spatial metabolic control: Rethinking DNMT1 targeting in MASLD: Letter to the editor on "DNMT1 facilitates the progression of MASLD by impeding transcription mediated by HNF4α and PPARα".Clinical and molecular hepatology · 2026Article
- Physical models reveal indirect reader protein interactions that facilitate epigenetic crosstalk.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Physical modeling of nucleosome clustering in euchromatin resulting from interactions between epigenetic reader proteins.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Two-way feedback between chromatin compaction and histone modification state explainsProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Polycomb repression of Hox genes involves spatial feedback but not domain compaction or phase transition.Nature genetics · 2024Article
- Computer simulations of chromatin phase separation.Biophysical journal · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We examine the relationship between the size of domains of epigenetic marks and the stability of those domains using our theoretical model that captures the physical mechanisms governing the maintenance of epigenetic modifications. We focus our study on histone H3 lysine-9 trimethylation, one of the most common and consequential epigenetic marks with roles in chromatin compaction and gene repression. Our model combines the effects of methyl spreading by methyltransferases and chromatin segregation into heterochromatin and euchromatin because of preferential heterochromatin protein 1 (HP1) binding. Our model indicates that, although large methylated domains are passed successfully from one chromatin generation to the next, small alterations to the methylation sequence are not maintained during chromatin replication. Using our predictive model, we investigate the size required for an epigenetic domain to persist over chromatin generations while surrounded by a much larger domain of opposite methylation and compaction state. We find that there is a critical size threshold in the hundreds-of-nucleosomes scale above which an epigenetic domain will be reliably maintained over generations. The precise size of the threshold differs for heterochromatic and euchromatic domains. Our results are consistent with natural alterations to the epigenetic sequence occurring during embryonic development and due to age-related epigenetic drift.
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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.