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PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE243334 | GEO | 2024/12/23

REPOSITORIES: GEO

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PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

Project description:the expression of TF MEF2C is decreased in skeletal muscle of PRR14-KO mice,which displays sarcopenia phenotype. Meanwhile, increasing MEF2C's expression in skeletal muscle lessens the phenotype.

2024-12-23 | GSE271657 | GEO

PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

Project description:Sarcopenia, characterized by the loss of muscle mass, strength, and function, predisposes adverse outcomes and its mechanism is waiting to reveal. Here, we report decrease of PRR14, a nuclear protein, in skeletal muscle results in sarcopenia. Genetically, genome-wide association studies (GWAS) identified multiple single nucleotide polymorphisms (SNPs) in PRR14 locus associated with body mass index (BMI) and total body lean mass, which indicated its association with sarcopenia; Specific knockout of skeletal muscle Prr14 in mice confirmed the causal effect; Biochemical analysis and high-throughput sequencing, including both transcriptome and approaches for the study of the epigenome (CUT&Tag sequencing and ATAC sequencing), revealed that Prr14 was required for myofiber homeostasis in skeletal muscle: Prr14 loss altered chromatin structure and reduced Mef2c activity, which in combination resulted in failure of maintaining myofiber identity and therefore sarcopenia. Our findings demonstrate that PRR14 orchestrates critical epigenetic changes and transcription factor activity to maintain myofiber identity, thereby providing novel therapeutic avenues for skeletal muscle pathologies associated with dysregulation of these mechanisms.

2024-12-23 | GSE243332 | GEO

PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

2024-12-23 | GSE243331 | GEO

PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

Project description:PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

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PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

Project description:PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

| PRJNA1017840 | ENA

PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

Project description:PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

| PRJNA1132706 | ENA

PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

Project description:PRR14 mediates mechanotransduction and regulates myofiber identity via MEF2C in skeletal muscle

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Foxj3 transcriptionally activates Mef2c and regulates adult skeletal muscle fiber type identity.

Project description:The mechanisms that regulate skeletal muscle differentiation, fiber type diversity and muscle regeneration are incompletely defined. Forkhead transcription factors are critical regulators of cellular fate determination, proliferation, and differentiation. We identified a forkhead/winged helix transcription factor, Foxj3, which was expressed in embryonic and adult skeletal muscle. To define the functional role of Foxj3, we examined Foxj3 mutant mice. Foxj3 mutant mice are viable but have significantly fewer Type I slow-twitch myofibers and have impaired skeletal muscle contractile function compared to their wild type controls. In response to a severe injury, Foxj3 mutant mice have impaired muscle regeneration. Foxj3 mutant myogenic progenitor cells have perturbed cell cycle kinetics and decreased expression of Mef2c. Examination of the skeletal muscle 5' upstream enhancer of the Mef2c gene revealed an evolutionary conserved forkhead binding site (FBS). Transcriptional assays in C2C12 myoblasts revealed that Foxj3 transcriptionally activates the Mef2c gene in a dose dependent fashion and binds to the conserved FBS. Together, these studies support the hypothesis that Foxj3 is an important regulator of myofiber identity and muscle regeneration through the transcriptional activation of the Mef2c gene.

| S-EPMC4540073 | biostudies-literature

MEF2C chip in the skeletal muscle of PRR14-KO mice

Project description:the expression and splice forms are regulated in the skeletal muscle of PRR14-KO mice, to explore the underlying mechanism of MEF2C-mediated PRR14's function in skeletal muscle, the chip assay was performed

2024-12-23 | GSE271658 | GEO

Alternative Splicing of Four Trafficking Genes Regulates Myofiber Structure and Skeletal Muscle Physiology.

Project description:During development, transcriptional and post-transcriptional networks are coordinately regulated to drive organ maturation. Alternative splicing contributes by producing temporal-specific protein isoforms. We previously found that genes undergoing splicing transitions during mouse postnatal heart development are enriched for vesicular trafficking and membrane dynamics functions. Here, we show that adult trafficking isoforms are also expressed in adult skeletal muscle and hypothesize that striated muscle utilizes alternative splicing to generate specific isoforms required for function of adult tissue. We deliver morpholinos into flexor digitorum brevis muscles in adult mice to redirect splicing of four trafficking genes to the fetal isoforms. The splicing switch results in multiple structural and functional defects, including transverse tubule (T-tubule) disruption and dihydropyridine receptor alpha (DHPR) and Ryr1 mislocalization, impairing excitation-contraction coupling, calcium handling, and force generation. The results demonstrate a previously unrecognized role for trafficking functions in adult muscle tissue homeostasis and a specific requirement for the adult splice variants.

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