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PLoS One. 2017 Aug 10;12(8):e0182568. doi: 10.1371/journal.pone.0182568. eCollection 2017.

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

Savol AJ1,2, Wang PI1,2, Jeon Y1,2,3, Colognori D1,2,3, Yildirim E1,2,3, Pinter SF1,2,3, Payer B1,2,3, Lee JT1,2,3, Sadreyev RI1,4.

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Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, United States of America.
Department of Genetics, Harvard Medical School, Boston, MA, United States of America.
Howard Hughes Medical Institute, Boston, MA, United States of America.
Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States of America.


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.

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