Imprinting control regions (ICRs) are marked by mono-allelic bivalent chromatin when transcriptionally inactive

Clicks: 85
ID: 282670
2018
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #263 of 803 articles by views in arXiv

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 803 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Parental allele-specific expression of imprinted genes is mediated by imprinting control regions (ICRs) that are constitutively marked by DNA methylation imprints on the maternal or paternal allele. Mono-allelic DNA methylation is strictly required for the process of imprinting and has to be faithfully maintained during the entire lifespan. While the regulation of DNA methylation itself is well understood, the mechanisms whereby the opposite allele remains unmethylated are unclear. Here, we show that in the mouse, at maternally methylated ICRs, the paternal allele, which is constitutively associated with H3K4me2/3, is marked by default by H3K27me3 when these ICRs are transcriptionally inactive, leading to the formation of a bivalent chromatin signature. Our data suggest that at ICRs, chromatin bivalency has a protective role by ensuring that DNA on the paternal allele remains unmethylated and protected against spurious and unscheduled gene expression. Moreover , they provide the proof of concept that, beside pluripotent cells, chromatin bivalency is the default state of transcriptionally inactive CpG island promoters , regardless of the developmental stage, thereby contributing to protect cell identity.
Reference Key
arnaud2018imprinting Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Stéphanie Maupetit-Méhouas; Bertille Montibus; David Nury; Chiharu Tayama; Michel Wassef; Satya Kota; Anne Fogli; Fabiana Cerqueira Campos; Kenichiro Hata; Robert Feil; Raphaël Margueron; Kazuhiko Nakabayashi; Franck Court; Philippe Arnaud
Journal arXiv
Year 2018
DOI
DOI not found
URL
http://arxiv.org/abs/1811.03952v1
Keywords
q-bio.mn q-bio.gn

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.