Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Affymetrix GeneChip Mouse Gene 1.0 arrays of RNA extracted from gastrocnemius muscle of 4 global Ppp3cb KO mice and 4 corresponding WT littermates, and 4 skeletal muscle-specific Ppp3r1Mlc1fCre KO and 4 corresponding WT littermates.

ABSTRACT: Global deficiency of catalytic subunit Ppp3cb, and tissue-specific ablation of regulatory subunit Ppp3r1 from skeletal muscle but not adipose tissue or liver led to protection from high-fat diet induced obesity and comorbid sequelæ. Ser637 hyperphosphorylation of dynamin-related protein 1 (Drp1) in skeletal muscle of calcineurin-deficient mice was associated with mitochondrial elongation into power-cable shaped filaments, increased mitochondrial respiration, but attenuated exercise performance.

ORGANISM(S): Mus musculus

PROVIDER: GSE71174 | GEO | 2015/07/22

SECONDARY ACCESSION(S): PRJNA290500

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Affymetrix GeneChip Mouse Gene 1.0 arrays of RNA extracted from gastrocnemius muscle of 4 global Ppp3cb KO mice and 4 corresponding WT littermates, and 4 skeletal muscle-specific Ppp3r1Mlc1fCre KO and 4 corresponding WT littermates.

Project description:Global deficiency of catalytic subunit Ppp3cb, and tissue-specific ablation of regulatory subunit Ppp3r1 from skeletal muscle but not adipose tissue or liver led to protection from high-fat diet induced obesity and comorbid sequelæ. Ser637 hyperphosphorylation of dynamin-related protein 1 (Drp1) in skeletal muscle of calcineurin-deficient mice was associated with mitochondrial elongation into power-cable shaped filaments, increased mitochondrial respiration, but attenuated exercise performance. Mice used for microarray analyses were all male, and chronically exposed to HFD for at least 8 weeks.

2015-07-22 | E-GEOD-71174 | biostudies-arrayexpress

Mitochondrial dynamics define muscle fiber type by modulating cellular metabolism pathways

Project description:Skeletal muscle is highly developed after birth, consisting of glycolytic fast- and oxidative slow-twitch fibers; however, the mechanisms of fiber type-specific differentiation are poorly understood. Here, we found an unexpected role for mitochondrial fission in the differentiation of fast-twitch oxidative fibers. Depletion of the mitochondrial fission factor dynamin-related protein 1 (Drp1) in mouse skeletal muscle and cultured myotubes resulted in the specific reduction of fast-twitch muscle fibers independently of respiratory function. Altered mitochondrial fission caused the activation of the Akt/mammalian target of rapamycin (mTOR) pathway via the mitochondrial accumulation of mTOR complex 2 (mTORC2), and rapamycin administration rescued the reduction of fast-twitch fibers in vivo and in vitro. Under Akt/mTOR activation, the mitochondria-related cytokine growth differentiation factor-15 was upregulated, which repressed fast-twitch fiber differentiation. Our findings reveal a novel role for mitochondrial dynamics in the activation of mTORC2 on mitochondria, resulting in the differentiation of muscle fibers.

2023-04-01 | GSE228362 | GEO

mRNAseq and proteomic data set of one week old WT (Chop wt/wt CkmmCre wt/wt Dars2 fl/fl), Chop KO (Chop ko/ko CkmmCre wt/wt Dars2 fl/fl), Dars2 KO (Chop wt/wt CkmmCre tg/wt Dars2 fl/fl) and DKO (Chop ko/ko CkmmCre tg/wt Dars2 fl/fl) mice

Project description:Maintenance of mitochondrial homeostasis is essential for a broad spectrum of signalling, metabolic and energetic processes. Consequently, mitochondrial dysfunction is linked to the development of a wide range of myopathies and many common diseases including type 2 diabetes, Parkinson’s and Alzheimer’s diseases. In response to disturbed mitochondrial proteostasis, an organelle-specific stress response is initiated, which results in a global adaptive transcriptional response partially sharing the signature of the integrated stress response (ISR). However, the exact sequence of events of the signalling cascade resulting in the activation of the ISR remains elusive. CHOP was the first transcription factor (TF) proposed to play a role in this process, although - due to the lack of a trans-activating domain - it needs to heterodimerize with other TFs to activate or suppresses its target genes. Therefore, we decided to investigate the molecular aspects and in vivo functions of CHOP in a murine model of mitochondrial dysfunction triggered by the loss of mitochondrial translation. Disruption of mitochondrial translation by heart and skeletal muscle-specific knock-out of the mitochondrial aspartyl-tRNA synthetase DARS2 on its own results in death of the animals within 7-8 weeks. Additional deletion of CHOP even further reduces the lifespan to less than 3 weeks, suggesting an existential role of the TF within the initiated stress signalling pathway. Our recent data indicates that CHOP's impact arises from the regulation of another TF with detrimental effects when exceedingly activated under certain circumstances: ATF4.

2022-04-04 | GSE149010 | GEO

Comparison of gene expression in skeletal muscle between Baf155 WT and mutant

Project description:Baf155 is a core subunit of SWI/SNF complex, an ATP dependent chromatin remodeler. To explore the function of Baf155 in skeletal muscle, we deleted the Baf155 in skeletal muscle and compared the gene expression profiling between wild type control and Baf155 deleted mutant mice.

2023-07-25 | GSE163373 | GEO

Proteomic analysis of single muscle fibres from WT and C18ORF25 KO mice

Project description:C18ORF25 is a homolog of Arkadia (RNF111), an E3 ubiquitin ligase with SUMO-interaction motifs (SIMs) (PMID: 31417085). However, C18ORF25 lacks the entire C-terminal RING domain of RNF111 which is required for ubiquitin binding suggesting it lacks ubiquitination activity and may therefore act as an adaptor or signalling scaffold (PMID: 26283374). We have previously shown that mice lacking C18Orf25 throughout the entire body have increased adiposity, decreased lean mass, lower exercise capacity and significantly reduced ex vivo skeletal muscle force production (PMID: 35882232). Skeletal muscle isolated from C18Orf25 knockout (KO) mice have reduced cAMP-dependent protein kinase A (PKA) levels, and reduced phosphorylation of several contractile proteins and proteins involved in calcium handling. Furthermore, analysis of single muscle fibres from C18Orf25 KO mice revealed impaired SR calcium cycling in fast-twitch fibres only (PMID: 35882232). Hence, we investigated these mechanisms by developing an integrated single-fibre physiology and single-fibre proteomic platform. The platform enabled us to identify hundreds of novel phenotype:protein correlations. The analysis also enabled us to identify proteome differences specifically in FT fibres following loss of C18ORF25. Taken together, our data suggest C18ORF25 is likely a multi-functional protein with several underlying mechanisms contributing to skeletal muscle physiology.

2024-01-03 | PXD045631 | Pride

RNA-sequencing of soleus muscle from Mustn1 heterozygous KO-first mice and wildtype littermates

Project description:To uncover novel genes and molecular pathways important for skeletal muscle remodeling and regeneration, we used a mouse hindlimb unloading and reloading protocol. We then performed analysis of global gene expression by RNA-sequencing (RNA-seq), looking at the transition from muscle unloading to reloading (GSE237099). This study focuses on the microprotein Mustn1 (Musculoskeletal embryonic nuclear protein 1, also known as Mustang), which consists of 82 amino acids. We performed RNA-sequencing of soleus muscle from 8-week-old mice carrying one allele (heterozygous) of Mustn1 tm1a (KO-first) and wildtype littermates.

2024-03-14 | GSE250506 | GEO

Muscle from patients with mitochondrial myopathies and congenital muscular dystrophies versus normal human muscle

Project description:Global gene expression analysis was performed comparing human skeletal muscle samples from patients with various forms of muscular dystrophy and mitochondrial myopathies in order to identify specific gene expression changes associated with collagen VI deficiency (leading to UllrichM-BM-4s Congenital Muscular Dystrophy) and depletion of mitochondrial DNA relative to other mitochondrial myopathies We analysed the gene expression profile of skeletal muscle from children suffering from mitochondrial myopathies and various forms of muscular dystrophy relative to skeletal muscle from healthy children using commercially available arrays that represents the complete human genome (Agilent Human SurePrintGE, 8x60K )

2015-01-20 | E-GEOD-43698 | biostudies-arrayexpress

RNA-seq of Mus musculus: WT and MTCH2 KO Naïve & Primed mouse embryonic stem cells

Project description:The role of mitochondria dynamics and its molecular regulators remains largely unknown during naïve-to-primed pluripotent cell interconversion. Here we report that mitochondrial MTCH2 is a regulator of mitochondrial fusion, essential for the naïve-to-primed interconversion of murine embryonic stem cells (ESCs). During this interconversion, wild-type ESCs elongate their mitochondria and slightly alter their glutamine utilization. In contrast, MTCH2-/- ESCs fail to elongate their mitochondria and to alter their metabolism, maintaining high levels of histone acetylation and expression of naïve pluripotency markers. Importantly, enforced mitochondria elongation by the pro-fusion protein Mitofusin (MFN) 2 or by a dominant negative form of the pro-fission protein dynamin-related protein (DRP) 1 is sufficient to drive the exit from naïve pluripotency of both MTCH2-/- and wild-type ESCs. Taken together, our data indicate that mitochondria elongation, governed by MTCH2, plays a critical role and constitutes an early driving force in the naïve-to-primed pluripotency interconversion of murine ESCs.

2018-11-10 | GSE122067 | GEO

Compensatory mechanisms in non-muscle organs in myotubular myopathy

Project description:X-Linked myotubular myopathy (XLMTM), is associated with very severe muscle weakness and reduced life expectancy. Liver dysfunction was also reported. The pathomechanism and the impact of non-muscular defects affecting survival are barely known. Here, we investigated organ-specific effects of XLMTM in the faithful Mtm1-/y mouse model. We performed RNA-sequencing to identify a shared mechanism in several skeletal muscles, and to investigate potential phenotypes and/or compensation in heart and liver. The cardiac and hepatic function and structural integrity were also studied in vivo and in vitro. There was no defect in liver function and morphology. A disease signature shared across several skeletal muscles including diaphragm highlighted dysregulations of muscle development, inflammation, cell adhesion and oxidative phosphorylation as main pathomechanisms. Heart displayed only slight functional alterations without obvious structural defects. An opposite dysregulation of specific pathways in cardiac compared to skeletal muscles was revealed at the transcriptome level. More specifically, biochemical and cellular experiments demonstrated that OXPHOS mitochondrial function, cell adhesion and beta integrin trafficking were strongly affected in skeletal muscle and normal in cardiac muscle. Moreover, biomarkers reflecting the molecular activity of MTM1, such as PtdIns3P and dynamin 2 levels, were increased in the skeletal muscles but not in cardiac muscle. Overall, these data identified a compensatory mechanism preserving cardiac function, indicating therapeutic targets to cure the severe skeletal muscle defects in XLMTM.

2024-12-18 | GSE242761 | GEO

Project description:Dynamin-related protein 1 regulates substrate oxidation in skeletal muscle by stabilizing cellular and mitochondrial calcium dynamics

| PRJNA684136 | ENA

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