Hyperactivation of HUSH complex function by Charcot-Marie-Tooth disease mutation in MORC2 View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-07

AUTHORS

Iva A Tchasovnikarova, Richard T Timms, Christopher H Douse, Rhys C Roberts, Gordon Dougan, Robert E Kingston, Yorgo Modis, Paul J Lehner

ABSTRACT

Dominant mutations in the MORC2 gene have recently been shown to cause axonal Charcot-Marie-Tooth (CMT) disease, but the cellular function of MORC2 is poorly understood. Here, through a genome-wide CRISPR-Cas9-mediated forward genetic screen, we identified MORC2 as an essential gene required for epigenetic silencing by the HUSH complex. HUSH recruits MORC2 to target sites in heterochromatin. We exploited a new method, differential viral accessibility (DIVA), to show that loss of MORC2 results in chromatin decompaction at these target loci, which is concomitant with a loss of H3K9me3 deposition and transcriptional derepression. The ATPase activity of MORC2 is critical for HUSH-mediated silencing, and the most common alteration affecting the ATPase domain in CMT patients (p.Arg252Trp) hyperactivates HUSH-mediated repression in neuronal cells. These data define a critical role for MORC2 in epigenetic silencing by the HUSH complex and provide a mechanistic basis underpinning the role of MORC2 mutations in CMT disease. More... »

PAGES

1035-1044

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ng.3878

    DOI

    http://dx.doi.org/10.1038/ng.3878

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1085864143

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28581500


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