Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional changes upon Mphosph8 or Morc2a loss in sorted neuronal nuclei of adult mouse brains.

ABSTRACT: We report that murine MPP8 and MORC2A are highly expressed in the brain and exclusively found in neurons. We show that genetic inactivation of Mphosph8 (coding for MPP8) or Morc2a in the nervous system of mice leads to alterations in brain architecture, behavioral impairments and reduction of life span. By doing RNA-seq and ChIP-seq experiments, we found that MPP8 and MORC2A suppress the repetitive-like protocadherin gene cluster on mouse chromosome 18 in a H3K9me3-dependent manner.

ORGANISM(S): Mus musculus

PROVIDER: GSE185329 | GEO | 2022/09/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide maps of H3K9me3 upon Mphosph8 or Morc2a loss in sorted neuronal nuclei of adult mouse brains.

Project description:We report that murine MPP8 and MORC2A are highly expressed in the brain and exclusively found in neurons. We show that genetic inactivation of Mphosph8 (coding for MPP8) or Morc2a in the nervous system of mice leads to alterations in brain architecture, behavioral impairments and reduction of life span. By doing RNA-seq and ChIP-seq experiments, we found that MPP8 and MORC2A suppress the repetitive-like protocadherin gene cluster on mouse chromosome 18 in a H3K9me3-dependent manner.

2022-09-13 | GSE189755 | GEO

Transcriptional changes upon Mphosph8 loss in mouse brains on postnatal day 14.

2022-09-13 | GSE185328 | GEO

Transcriptional changes upon Mphosph8 or Morc2a loss

Project description:Transcriptional changes upon Mphosph8 or Morc2a loss

| PRJNA768763 | ENA

ChIP-seq analysis of H3K4me3, H3K9me3 and MPHOSPH8 in MOLM-13 cells

Project description:Human cancers including acute myeloid leukemia (AML) hijack epigenetic machinery to drive malignant self-renewal, whereas dysregulated epigenetic states also create selective and targetable liabilities. We performed domain-based CRISPR/Cas9 screens of human chromatin regulators and identified MPHOSPH8 (or MPP8), a component of the HUSH complex and repressor of LINE-1 retrotransposons, as a selective epigenetic dependency of AML cells. While dispensable for normal hematopoiesis, MPP8 loss inhibited AML initiation and maintenance by reactivating LINE-1 retrotransposons. Activation of endogenous or ectopic LINE-1 photocopied MPP8 loss, whereas blocking LINE-1 retrotransposition abrogated MPP8-deficiency-induced phenotypes. Reactivated LINE-1 retrotransposition increased DNA damage, activated cyclin-dependent kinase inhibitor p21 (or CDKN1A), and induced AML differentiation. Enhanced L1 suppression in AML stem cells is associated with therapy resistance and poor prognosis. Hence, while retrotransposons are historically recognized as sources of genetic instability and somatic mutations, we uncover an unexpected role for HUSH/MPP8 in promoting cancer by suppressing genomic transposable elements.

2021-02-01 | GSE150981 | GEO

RNA-seq analysis of transcriptomic changes in WT and MPHOSPH8 KO MOLM-13 leukemia cells

2021-02-01 | GSE150982 | GEO

Transcriptional changes upon Mphosph8 or Morc2a loss in sorted neuronal nuclei of adult mouse brains.

Project description:Transcriptional changes upon Mphosph8 or Morc2a loss in sorted neuronal nuclei of adult mouse brains.

| PRJNA768771 | ENA

Gene expression profile at single cell level of human control, MPHOSPH8-deficient and MORC2-deficient cerebral organoids at day 27.

Project description:To translate our mouse data and to model the role of MPHOSPH8 and MORC2 in human brain development, we generated human three-dimensional (3D) cerebral organoids lacking MPHOSPH8 and MORC2. These cerebral organoids were compared to control organoids by single cell RNA sequencing (scRNA-seq) to analyze the cell composition and expression of clustered protocadherins.

2024-10-18 | GSE279721 | GEO

Genome-wide maps of H3K9me3 upon Mphosph8 or Morc2a loss in sorted neuronal nuclei of adult mouse brains.

Project description:Genome-wide maps of H3K9me3 upon Mphosph8 or Morc2a loss in sorted neuronal nuclei of adult mouse brains.

| PRJNA784423 | ENA

Analysis of MPHOSPH8 chromatin occupancy and MPHOSPH8-dependent gene expression in MOLM-13 leukemia cells

Project description:Analysis of MPHOSPH8 chromatin occupancy and MPHOSPH8-dependent gene expression in MOLM-13 leukemia cells

| PRJNA634314 | ENA

Morc2a variants cause hydroxyl radical-mediated neuropathy and are rescued by GHKL ATPase gene therapy

Project description:Mutations in the Microrchidia CW-Type Zinc Finger 2 (MORC2) GHKL ATPase module cause Charcot Marie Tooth type 2Z or a broad range of neuropathy, but etiology and therapeutic strategy are not fully defined. Previously, we reported that the Morc2a p.S87L mouse model led to neuropathy and muscular dysfunction through DNA damage accumulation. This study revealed that Morc2a p.S87L caused a protein synthesis defect, resulting in the loss of function of Morc2a and weakening its function of maintaining DNA integrity and hydroxyl radical scavenging in the GHKL ATPase domain. Morc2a GHKL ATPase domain was considered a therapeutic target based on its function of simultaneously complementing hydroxyl radical scavenging and ATPase activity. Adeno-associated virus PHP.eB serotype that has high central nervous system transduction efficiency was applied to express Morc2a or Morc2a GHKL ATPase domain protein in vivo. AAV gene therapy improved neuropathy and muscular dysfunction with single-time treatment. The loss of function characteristics due to protein synthesis defect in Morc2a p.S87L was also observed in human MORC2 p.S87L or p.R252W variant, suggesting a relevance between mouse and human pathogenesis. Here, we demonstrate Morc2a p.S87L variant causes hydroxyl radical-mediated neuropathy and could be rescued through AAV-based gene therapy.

2024-02-06 | GSE235918 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data