Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of wild-type and mfn1-/-,mfn2-/- tibialis anterior muscle (mouse).

ABSTRACT: We report the transcriptome changes in tibialis anterior muscle in response to deletion of the Mfn1 and Mfn2 genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE198071 | GEO | 2022/03/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq of wild-type and mfn1-/-,mfn2-/- tibialis anterior muscle (mouse).

Project description:RNA-seq of wild-type and mfn1-/-,mfn2-/- tibialis anterior muscle (mouse).

| PRJNA813566 | ENA

RNA sequencing of pancreatic islets from WT, Mfn1-/-, Mfn2-/- and Mfn1/2-/- mice

Project description:The dynamin-like GTPases Mitofusin 1 and 2 (Mfn1 and Mfn2) are essential for mitochondrial function, which has been principally attributed to their regulation of fission/fusion dynamics. Here, we report that Mfn1 and 2 are critical for glucose-stimulated insulin secretion (GSIS) primarily through control of mtDNA content. Whereas Mfn1 and Mfn2 individually were dispensable for glucose homeostasis, combined Mfn1/2 deletion in β-cells reduced mtDNA content, induced impaired mitochondrial morphology and networking fragmentation, and impaired decreased respiratory function, ultimately resulting in severe glucose intolerance. Importantly, gene dosage studies unexpectedly revealed that Mfn1/2 control of glucose homeostasis was dependent on maintenance of mtDNA content, rather than mitochondrial structure. Indeed, pharmacologic mitofusin agonists rescued islet mtDNA depletion due to mitofusin deficiency independent of changes on mitochondrial structure. Mfn1/2 maintain mtDNA content by regulating the expression of the crucial mitochondrial transcription factor Tfam, as Tfam overexpression ameliorated the reduction in mtDNA content and GSIS in Mfn1/2-deficient β-cells. Thus, the primary physiologic role of Mfn1 and 2 in β-cells is coupled to preservation of mtDNA content rather than mitochondrial architecture, and Mfn1 and 2 may be promising targets to overcome mitochondrial dysfunction and restore glucose control in diabetes.

2022-02-16 | GSE194204 | GEO

Endogenous interactomes of MFN1 and MFN2 provide novel insights into interorganelle communication and autophagy

Project description:Mitofusin-1 (MFN1) and Mitofusin-2 (MFN2) are key players in mitochondrial fusion, endoplasmic reticulum (ER)-mitochondria yuxtaposition, and autophagy. However, the mechanisms by which these proteins participate in these processes remain poorly understood. To better understand their functions, we studied the interactomes of these two proteins. To this end, we used CRISPR/Cas9 technology to insert an HA-tag in the C-terminal domain of MFN1 and MFN2 and generated HeLa cell lines that endogenously expressed MFN1-HA or MFN2-HA, respectively. HA-pulldown followed by mass spectrometry identified potential interactors of MFN1 and MFN2. A substantial proportion of interactors were common for MFN1 and MFN2 and were regulated by nutrient deprivation. We validated novel ER and endosomal partners of MFN1 and/or MFN2 with a potential role in interorganelle communication. We characterized RAB5C as an endosomal modulator of mitochondrial dynamics through its interaction with MFN1 and SLC27A2 as a novel partner of MFN2 relevant in autophagy. Our findings reveal that MFN proteins participate in nutrient-modulated pathways involved in organelle communication.

2025-07-16 | PXD043168 | Pride

Nr2f6 electroporation in tibialis anterior promotes muscle weakness

Project description:Mouse tibialis anterior muscles were electroporated with Nr2f6-myc plasmid or pCMV6 empty vector in the contralateral leg. After 9 days, muscles were collected, and the RNA extracted and processed for microarray analysis.

2024-03-31 | GSE228202 | GEO

RNA sequencing of pancreatic islets from WT, Mfn1-/-, Mfn2-/- and Mfn1/2-/- mice

Project description:RNA sequencing of pancreatic islets from WT, Mfn1-/-, Mfn2-/- and Mfn1/2-/- mice

| PRJNA799610 | ENA

RNAseq from Mfn1/2 knockout MEFs with adipogenic differentiation

Project description:Objective: A biallelic missense mutation in mitofusin 2 (MFN2) causes multiple symmetric lipomatosis and partial lipodystrophy, implicating disruption of mitochondrial fusion or interaction with other organelles in adipocyte differentiation, growth and/or survival. In this study, we aimed to document the impact of loss of mitofusin 1 (Mfn1) or 2 (Mfn2) on adipogenesis in cultured cells. Methods: We characterised adipocyte differentiation of wildtype (WT), Mfn1-/- and Mfn2-/- mouse embryonic fibroblasts (MEFs) and 3T3-L1 preadipocytes in which Mfn1 or 2 levels were reduced using siRNA. Results: Mfn1-/- MEFs displayed striking fragmentation of the mitochondrial network, with surprisingly enhanced propensity to differentiate into adipocytes, as assessed by lipid accumulation, expression of adipocyte markers (Plin1, Fabp4, Glut4, Adipoq), and insulin-stimulated glucose uptake. RNA sequencing revealed a corresponding pro-adipogenic transcriptional profile including Pparg upregulation. Mfn2-/- MEFs also had a disrupted mitochondrial morphology, but in contrast to Mfn1-/- MEFs they showed reduced expression of adipocyte markers. Mfn1 and Mfn2 siRNA mediated knockdown studies in 3T3-L1 adipocytes generally replicated these findings. Conclusions: Loss of Mfn1 but not Mfn2 in cultured pre-adipocyte models is pro-adipogenic. This suggests distinct, non-redundant roles for the two mitofusin orthologues in adipocyte differentiation.

2023-06-01 | GSE232502 | GEO

Expression data from tibialis anterior muscle

Project description:We generated transgenic mice expressing constitutively SOCS-3 specifically in skeletal muscle. SOCS proteins are implicated in the negative regulation of various pathways including insulin signaling pathway. Our transgenic mice are predisposed to obesity and systemic insulin resistance compared to control mice. We used microarrays to detail the variations of gene expression in muscle from transgenic mice versus controls. Keywords: transgenic, tibialis anterior, SOCS-3

2009-03-01 | GSE11105 | GEO

Analysis of tibialis anterior muscle post-injection with nanoparticles in mice

Project description:Proteomic study of tibialis anterior muscle harvested at 1 day and 7 days post-injection with novel polyurethane nanoparticles compared to water sham and non-injected controls

2021-03-12 | MSV000087040 | MassIVE

Nr2f6 electroporation in tibialis anterior promotes muscle weakness

Project description:Nr2f6 electroporation in tibialis anterior promotes muscle weakness

| PRJNA948669 | ENA

Tibialis anterior muscle of myostatin null mice treated with clenbuterol

Project description:Transcription profiling of skeletal muscle (tibialis anterior) of 5-week-old male wild type and myostatin null mice given ad libitum access to 20ppm clenbuterol hydrochloride in drinking water or plain tap water for 2 weeks. The objective of the study was to determine overlap in the mechanisms of muscle hypertrophy of the two models.

2014-02-03 | GSE27577 | 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