Genome-wide identification of autosomal genes with allelic imbalance of chromatin state.

In mammals, monoallelic gene expression can result from X-chromosome inactivation, genomic imprinting, and random monoallelic expression (RMAE). Epigenetic regulation of RMAE is not fully understood. Here we analyze allelic imbalance in chromatin state of autosomal genes using ChIP-seq in a clonal c...

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Main Authors: Andrej J Savol, Peggy I Wang, Yesu Jeon, David Colognori, Eda Yildirim, Stefan F Pinter, Bernhard Payer, Jeannie T Lee, Ruslan I Sadreyev
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2017-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC5552117?pdf=render
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spelling doaj-d2fb6aac590144e1a7065ef3104958b42020-11-25T02:05:48ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01128e018256810.1371/journal.pone.0182568Genome-wide identification of autosomal genes with allelic imbalance of chromatin state.Andrej J SavolPeggy I WangYesu JeonDavid ColognoriEda YildirimStefan F PinterBernhard PayerJeannie T LeeRuslan I SadreyevIn mammals, monoallelic gene expression can result from X-chromosome inactivation, genomic imprinting, and random monoallelic expression (RMAE). Epigenetic regulation of RMAE is not fully understood. Here we analyze allelic imbalance in chromatin state of autosomal genes using ChIP-seq in a clonal cell line. We identify approximately 3.7% of autosomal genes that show significant differences between chromatin states of two alleles. Allelic regulation is represented among several functional gene categories including histones, chromatin modifiers, and multiple early developmental regulators. Most cases of allelic skew are produced by quantitative differences between two allelic chromatic states that belong to the same gross type (active, silent, or bivalent). Combinations of allelic states of different types are possible but less frequent. When different chromatin marks are skewed on the same gene, their skew is coordinated as a result of quantitative relationships between these marks on each individual allele. Finally, combination of allele-specific densities of chromatin marks is a quantitative predictor of allelic skew in gene expression.http://europepmc.org/articles/PMC5552117?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Andrej J Savol
Peggy I Wang
Yesu Jeon
David Colognori
Eda Yildirim
Stefan F Pinter
Bernhard Payer
Jeannie T Lee
Ruslan I Sadreyev
spellingShingle Andrej J Savol
Peggy I Wang
Yesu Jeon
David Colognori
Eda Yildirim
Stefan F Pinter
Bernhard Payer
Jeannie T Lee
Ruslan I Sadreyev
Genome-wide identification of autosomal genes with allelic imbalance of chromatin state.
PLoS ONE
author_facet Andrej J Savol
Peggy I Wang
Yesu Jeon
David Colognori
Eda Yildirim
Stefan F Pinter
Bernhard Payer
Jeannie T Lee
Ruslan I Sadreyev
author_sort Andrej J Savol
title Genome-wide identification of autosomal genes with allelic imbalance of chromatin state.
title_short Genome-wide identification of autosomal genes with allelic imbalance of chromatin state.
title_full Genome-wide identification of autosomal genes with allelic imbalance of chromatin state.
title_fullStr Genome-wide identification of autosomal genes with allelic imbalance of chromatin state.
title_full_unstemmed Genome-wide identification of autosomal genes with allelic imbalance of chromatin state.
title_sort genome-wide identification of autosomal genes with allelic imbalance of chromatin state.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2017-01-01
description In mammals, monoallelic gene expression can result from X-chromosome inactivation, genomic imprinting, and random monoallelic expression (RMAE). Epigenetic regulation of RMAE is not fully understood. Here we analyze allelic imbalance in chromatin state of autosomal genes using ChIP-seq in a clonal cell line. We identify approximately 3.7% of autosomal genes that show significant differences between chromatin states of two alleles. Allelic regulation is represented among several functional gene categories including histones, chromatin modifiers, and multiple early developmental regulators. Most cases of allelic skew are produced by quantitative differences between two allelic chromatic states that belong to the same gross type (active, silent, or bivalent). Combinations of allelic states of different types are possible but less frequent. When different chromatin marks are skewed on the same gene, their skew is coordinated as a result of quantitative relationships between these marks on each individual allele. Finally, combination of allele-specific densities of chromatin marks is a quantitative predictor of allelic skew in gene expression.
url http://europepmc.org/articles/PMC5552117?pdf=render
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