Dataset Information


Assessing the impact of the R252W Charcot-Marie-Tooth disease mutation in MORC2 on HUSH-mediated repression

ABSTRACT: HeLa cells lacking MORC2 generated through CRISPR/Cas9-mediated gene disruption were reconstituted with either wild-type or R252W mutant MORC2, and re-repression of HUSH target genes assessed by RNA-seq Overall design: Total RNA-seq of MORC2 knockout cells, either 1) mock transduced, 2) transduced with lentiviral vector encoding wild-type MORC2 or 3) transduced with lentviral vector encoding R252W MORC2.

INSTRUMENT(S): Illumina HiSeq 2500 (Homo sapiens)

SUBMITTER: Iva Tchasovnikarova  

PROVIDER: GSE95455 | GEO | 2017-05-29



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Hyperactivation of HUSH complex function by Charcot-Marie-Tooth disease mutation in MORC2.

Tchasovnikarova Iva A IA   Timms Richard T RT   Douse Christopher H CH   Roberts Rhys C RC   Dougan Gordon G   Kingston Robert E RE   Modis Yorgo Y   Lehner Paul J PJ  

Nature genetics 20170605 7

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  ...[more]

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