Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE95455 | GEO | 2017/05/29

SECONDARY ACCESSION(S): PRJNA377249

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Hyper-repression of HUSH target genes by over-expression of the R252W Charcot-Marie-Tooth disease mutant MORC2

Project description:By comparing wild-type SK-N-SH neuroblastoma cells to cells over-expressing either wild-type or R252W mutant MORC2, the goal of the experiment was to assess the effect of MORC2 over-expression on the transcriptome.

2017-05-29 | GSE95453 | GEO

Hyper-activation of HUSH complex function by Charcot-Marie-Tooth disease mutation in MORC2

Project description:Hyper-activation of HUSH complex function by Charcot-Marie-Tooth disease mutation in MORC2

| PRJNA377238 | ENA

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

Project description: Not available

| S-EPMC5493197 | biostudies-literature

Assessing the genome-wide occupancy of MORC2

Project description: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.

2017-05-29 | GSE95451 | GEO

DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex

Project description:The human silencing hub (HUSH) complex binds to transcripts of LINE-1 retrotransposons (L1s) and other genomic repeats, recruiting MORC2 and other effectors to remodel chromatin. However, how HUSH and MORC2 operate alongside DNA methylation, a central epigenetic regulator of repeat transcription, remains poorly understood. Here we interrogate this relationship in human neural progenitor cells (hNPCs), a somatic model of brain development that tolerates removal of DNA methyltransferase DNMT1. Upon loss of MORC2 or HUSH subunit TASOR in hNPCs, L1s remain silenced by robust promoter methylation. However, genome demethylation and activation of evolutionarily-young L1s attracts MORC2 binding. Simultaneous depletion of DNMT1 and MORC2 causes massive accumulation of L1 transcripts. We identify the same mechanistic hierarchy at pericentromeric α-satellites and clustered protocadherin genes, repetitive elements important for chromosome structure and neurodevelopment respectively. Our data delineate the independent epigenetic control of repeats in somatic cells, with implications for understanding the vital functions of HUSH-MORC2 in hypomethylated contexts throughout human development.

2024-03-26 | GSE242143 | GEO

DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex [CUT&RUN]

2024-03-26 | GSE240384 | GEO

DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex [Bulk RNA-seq]

2024-03-26 | GSE240386 | GEO

DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex [ONT cDNA sequencing]

2024-03-26 | GSE262483 | GEO

DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex [ONT whole genome DNA]

2024-03-26 | GSE262482 | GEO

Hyper-activation of HUSH complex function by Charcot-Marie-Tooth disease mutation in MORC2

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-05-29 | GSE95480 | GEO