Genomics

Dataset Information

147

Assessing the genome-wide occupancy of MORC2


ABSTRACT: By comparing HeLa cells expressing V5 epitope-tagged MORC2 constructs, the goal of the experiment was to determine the genome-wide localisation of MORC2 in the presence or absence of the HUSH complex and upon inactivation of the CW domain. The occupancy of V5-MORC2 was also compared to that of endogenous TASOR. Overall design: ChIP-seq analysis of endogenous TASOR and IgG control in wild-type HeLa cells. ChIP-seq analysis of V5 epitope-tagged wild-type MORC2 and the CW domain mutant W505A expressed in MORC2 knockout HeLa cells generated through CRISPR/Cas9-mediated gene disruption. In parallel, ChIP-seq analysis of V5 epitope-tagged MORC2 in HUSH tirple knockout cells was also carried out.

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

SUBMITTER: Iva Tchasovnikarova  

PROVIDER: GSE95451 | GEO | 2017-05-29

SECONDARY ACCESSION(S): PRJNA377245

REPOSITORIES: GEO

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Publications

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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