Locus specific epigenetic modalities of random allelic expression imbalance

Lucile Marion-Poll (), Benjamin Forêt, Dina Zielinski, Florian Massip, Mikael Attia, Ava C. Carter, Laurène Syx, Howard Y. Chang, Anne-Valerie Gendrel () and Edith Heard ()
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Lucile Marion-Poll: Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934
Benjamin Forêt: Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934
Dina Zielinski: Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934
Florian Massip: Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine
Mikael Attia: Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934
Ava C. Carter: Stanford University
Laurène Syx: Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934
Howard Y. Chang: Stanford University
Anne-Valerie Gendrel: Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934
Edith Heard: Institut Curie, PSL Research University, CNRS UMR3215, INSERM U934

Nature Communications, 2021, vol. 12, issue 1, 1-14

Abstract: Abstract Most autosomal genes are thought to be expressed from both alleles, with some notable exceptions, including imprinted genes and genes showing random monoallelic expression (RME). The extent and nature of RME has been the subject of debate. Here we investigate the expression of several candidate RME genes in F1 hybrid mouse cells before and after differentiation, to define how they become persistently, monoallelically expressed. Clonal monoallelic expression is not present in embryonic stem cells, but we observe high frequencies of monoallelism in neuronal progenitor cells by assessing expression status in more than 200 clones. We uncover unforeseen modes of allelic expression that appear to be gene-specific and epigenetically regulated. This non-canonical allelic regulation has important implications for development and disease, including autosomal dominant disorders and opens up therapeutic perspectives.

Date: 2021
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DOI: 10.1038/s41467-021-25630-3

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