ArticleCell cycle (Georgetown, Tex.)2012
Concerted epigenetic signatures inheritance at PcG targets through replication.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Nuclear Mechanics and Nuclear Mechanotransduction in Cancer Cell Migration and Invasion.Biomolecules · 2026Review
- Polycomb Bodies Detection in Murine Fibromuscular Stroma from Skin, Skeletal Muscles, and Aortic Tissues.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Alternative models for transgenerational epigenetic inheritance: Molecular psychiatry beyond mice and man.World journal of psychiatry · 2021Review
- Nucleoplasmic Lamin A/C and Polycomb group of proteins: An evolutionarily conserved interplay.Nucleus (Austin, Tex.) · 2016Article
- Mariner Transposons Contain a Silencer: Possible Role of the Polycomb Repressive Complex 2.PLoS genetics · 2016Article
- Review
- What are memories made of? How Polycomb and Trithorax proteins mediate epigenetic memory.Nature reviews. Molecular cell biology · 2014Review
- How is epigenetic information maintained through DNA replication?Epigenetics & chromatin · 2013Article
- PcG-mediated higher-order chromatin structures modulate replication programs at the Drosophila BX-C.PLoS genetics · 2013Article
- Protocol: Chromatin immunoprecipitation (ChIP) methodology to investigate histone modifications in two model diatom species.Plant methods · 2012Article
- Epigenetic alterations in muscular disorders.Comparative and functional genomics · 2012Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Polycomb group of proteins (PcG), by controlling gene silencing transcriptional programs through cell cycle, lock cell identity and memory. Recent chromatin genome-wide studies indicate that PcG targets sites are bivalent domains with overlapping repressive H3K27me3 and active H3K4me3 mark domains. During S phase, the stability of epigenetic signatures is challenged by the replication fork passage. Hence, specific mechanisms of epigenetic inheritance might be provided to preserve epigenome structures. Recently, we have identified a critical time window before replication, during which high levels of PcG binding and histone marks on BX-C PRE target sites set the stage for subsequent dilution of epigenomic components, allowing proper transmission of epigenetic signatures to the next generation. Here, we extended this analysis to promoter elements, showing the same mechanism of inheritance. Furthermore, to gain insight into the inheritance of PREs bivalent marks, we analyzed dynamics of H3K4me3 deposition, a mark that correlates with transcriptionally active chromatin. Likewise, we found an early S-phase enrichment of H3K4me3 mark preceding the replication-dependent dilution. This evidence suggests that all epigenetic marks are inherited simultaneously to ensure their correct propagation through replication and to protect the "bivalency" of PREs.
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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.