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Analysis of gastrocnemius muscle from chow-fed control and skeletal muscle specific Cpt1b knockout mice

ABSTRACT: Analysis of gastrocnemius muscle from chow-fed control and skeletal muscle specific Cpt1b knockout mice

PROVIDER: PRJNA419145 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6308330.fastq.gz	Fastqsanger.gz
	SRR6308331.fastq.gz	Fastqsanger.gz
	SRR6308332.fastq.gz	Fastqsanger.gz
	SRR6308323.fastq.gz	Fastqsanger.gz
	SRR6308333.fastq.gz	Fastqsanger.gz

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Analysis of gastrocnemius muscle from chow-fed control and skeletal muscle specific Cpt1b knockout mice

Project description:To determine the transcriptomic effects of Cpt1b loss on skeletal muscle gene expression, we assessed gastrocnemius muscle in chow-fed control and Cpt1b skeletal muscle specific knockout mice using a serial analysis of gene expression strategy. Complementary bioinformatics pathway enrichment studies were performed which indicated that differentially expressed genes between genotypes were predominantly related to various processes include carbohydrate metabolism, lipid metabolism, amino acid metabolism, cell proliferation, and apoptosis.

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Analysis of gastrocnemius muscle from chow-fed control and UCP1 knockout rats at room temperature and after exposure to 4 degrees Celsius

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Project description:The processes by which mitochondria respond to cellular energy demands brought on by physiologic and pathophysiologic stimuli are essential to cellular adaptation and organismal survival. Disrupted mitochondrial function is implicated in several human disease states, underscoring the need to elucidate the molecular mechanisms that control mitochondrial function and metabolism. We previously described a patient with a gain-of-function mutation in Site-1 Protease (S1P) who exhibited idiopathic hyperCKemia, myoedema, and altered muscle mitochondrial morphology. To date, S1P has been heavily characterized in liver and bone, with very little known about its potential function in skeletal muscle. In our current study, we generated a skeletal muscle-specific S1P knockout mouse line (S1PsmKO) to examine the role of S1P in skeletal muscle. S1PsmKO mice were overtly normal in their appearance and health. However, examination of 12-week-old S1PsmKO mice showed increased gastrocnemius muscle mass and aged S1PsmKO mice exhibited increased muscle mass in both gastrocnemius and soleus relative to age-matched controls. Moreover, isolated muscle from S1PsmKO exhibited increased maximal mitochondrial respiration relative to floxed littermates (controls). RNA-Seq analysis showed increased transcript numbers of the mitochondrial-resident gene, Mss51 in S1PsmKO gastrocnemius relative to control mice. Mss51 is a member of the TGF-β/MSTN pathway, which controls mitochondrial metabolism. Similar to S1PsmKO muscle, S1P-depleted C2C12 cells also had increased maximal respiration, which was reversed by exogenous MSS51 expression. These data identify S1P as a regulator of muscle mass and mitochondrial metabolism, and implicate S1P as a novel modulator of TGF-β signaling. Method: Male mice were maintained on standard chow diet until 12 weeks of age.

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