Effect of USP21 deficiency on transcriptomes in skeletal muscle of mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA669695 | ENA |
REPOSITORIES: ENA
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Project description:Skeletal muscle is the pivotal organ for energy homeostasis, but the regulatory mechanisms are largely unknown. Here, we report that ubiquitin specific protease 21 (USP21) is a regulator of skeletal muscle physiology. To elucidate features important for USP21, we performed RNA-sequencing analysis using the muscle tissue of muscle-specific USP21 knockout (USP21-MKO) mice or wild-type littermates with floxed genotype, screened and analyzed the differentially expressed genes. Transcriptomics assay enabled us to discover major signaling nodes persistently activated by USP21 ablation in close association with the genes linked to fuel oxidation. Consequently, USP21 ablation altered gross metabolic phenotypes.
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Project description:Expanding the exercise capacity is an emerging strategy to combat metabolic diseases. Skeletal muscle fiber type determination is critical for the exercise performance, but the regulatory basis is largely unknown. Here, we report that Sirt6 has a role in regulating myofiber configuration toward oxidative type and that Sirt6 activator can be an exercise mimetic. To elucidate molecular mechanisms, we performed RNA-sequencing analysis using WT and skeletal muscle-specific Sirt6 KO mice. Transcriptomic analysis enabled us to discover major signaling nodes altered by Sirt6 deficiency in close association with mitochondrial function and muscle phenotypes.
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Project description:Nebulin is a giant filamentous protein that is coextensive with the actin filaments of the skeletal muscle sarcomere. Nebulin mutations are the main cause of nemaline myopathy (NEM), with typical NEM adult patients having low expression of nebulin, yet the roles of nebulin in adult muscle remain poorly understood. To establish nebulin’s functional roles in adult muscle we performed studies on a novel conditional nebulin KO (Neb cKO) mouse model in which nebulin deletion was driven by the muscle creatine kinase (MCK) promotor. Neb cKO mice are born with high nebulin levels in their skeletal muscle but within weeks after birth nebulin expression rapidly falls to barely detectable levels Surprisingly, a large fraction of the mice survives to adulthood with low nebulin levels (<5% of control), contain nemaline rods, and undergo fiber-type switching towards oxidative types. These microarrays investigate the changes in gene expression when nebulin is deficient. Two skeletal muscle groups were studied: Quadriceps (which is markedly smaller in the Neb cKO mice relative to control) and Soleus (which is not significantly smaller in the Neb cKO relative to control). Six biological replicates for each muscle group were selected; all are age-matched males.
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Project description:Mitochondria serve diverse functions and are essential organelles that require continuous surveillance to maintaintheir integrity and function. LONP1 is an evolutionarily conservedserine peptidase that safeguards mitochondrial protein quality from yeast to human.To investigatethe physiological role of LONP1-mediated mitochondrial quality-control in skeletal musclein vivo, we generated skeletal muscle-specificLonp1-knockout mice (referred to as LONP1 MKO). We performedtranscriptome analysis by whole-genome gene expression profiling experiments in gastrocnemius (GC) muscle from both wild-type (WT) and LONP1-MKO mice. Knockout of LONP1 in skeletal muscle resulted in deregulation of 457 genes in 2-week-old mice and of 1922 genes in 6-week-old mice. Gene ontology analysis revealed that LONP1 deficiency triggers unfolded protein response (UPR) in skeletal muscle.Moreover, GSEA analysis of transcriptomic datain 6-week-old micefurther revealed that genes deregulated by LONP1 deficiency were significantly enriched during aging.Together, the transcriptional profiling results suggest a critical role of LONP1 in regulating skeletal muscle metabolism and health.
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Project description:Nebulin is a giant filamentous protein that is coextensive with the actin filaments of the skeletal muscle sarcomere. Nebulin mutations are the main cause of nemaline myopathy (NEM), with typical NEM adult patients having low expression of nebulin, yet the roles of nebulin in adult muscle remain poorly understood. To establish nebulin’s functional roles in adult muscle we performed studies on a novel conditional nebulin KO (Neb cKO) mouse model in which nebulin deletion was driven by the muscle creatine kinase (MCK) promotor. Neb cKO mice are born with high nebulin levels in their skeletal muscle but within weeks after birth nebulin expression rapidly falls to barely detectable levels Surprisingly, a large fraction of the mice survives to adulthood with low nebulin levels (<5% of control), contain nemaline rods, and undergo fiber-type switching towards oxidative types. These microarrays investigate the changes in gene expression when nebulin is deficient.
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Project description:Obesity-related muscular dysfunction and relative muscle atrophy affect an increasing number of people. Elucidating the molecular mechanisms of skeletal muscle cell development and growth may contribute to the maintenance of skeletal muscle mass in obesity. Fatty acid translocase (FAT/CD36), as a long-chain fatty acid transport protein, is crucial for lipid metabolism and signaling. CD36 is known to function in myogenic differentiation, and whether it affects the proliferation of skeletal muscle cells and the underlying mechanisms remain unclear. In this study, the effect of CD36 deficiency on skeletal muscle cell viability and proliferation was examined using C2C12 myoblasts. Results showed that the deletion of CD36 enhanced the inhibitory effect of PA on the proliferation and the promotion of apoptosis in skeletal muscle cells. Intriguingly, the silencing of CD36 suppressed cell proliferation by preventing the cell cycle from the G0/G1 phase to the S phase in a cyclin D1/CDK4-dependent manner. Overall, we demonstrated that CD36 was involved in skeletal muscle cell proliferation by cell cycle control, and these findings might facilitate the treatment of obesity-related muscle wasting.
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