ArticleCell death and differentiation2025
Adapting cytoskeleton-mitochondria patterning with myocyte differentiation by promyogenic PRR33.
Article in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Immunomodulatory cytoskeleton of bionic periosteum affects mitochondrial dynamics to promote osteogenesis.Bioactive materials · 2026Article
- Angiogenin mediates cell-cell fusion as a mitochondrial RNA processing enzyme.Bone research · 2026Article
- Transcriptome Sequencing and Differential Analysis of Testes in One- and Two-Year-Old Kazakh Horses.Animals : an open access journal from MDPI · 2026Article
- Estrogen-Related Receptor Alpha Promotes Skeletal Muscle Regeneration and Mitigates Muscular Dystrophy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Transcriptome Analysis of Muscle Tissue from Three Anatomical Locations in Male and Female Kazakh Horses.Biology · 2025Article
- Transcriptomic sequencing and differential analysis of Kazakh horse muscles from various anatomical locations.Frontiers in veterinary science · 2025Article
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Authors and funding
19 authors.
Funding
Abstract
Coordinated cytoskeleton-mitochondria organization during myogenesis is crucial for muscle development and function. Our understanding of the underlying regulatory mechanisms remains inadequate. Here, we identified a novel muscle-enriched protein, PRR33, which is upregulated during myogenesis and acts as a promyogenic factor. Depletion of Prr33 in C2C12 represses myoblast differentiation. Genetic deletion of Prr33 in mice reduces myofiber size and decreases muscle strength. The Prr33 mutant mice also exhibit impaired myogenesis and defects in muscle regeneration in response to injury. Interactome and transcriptome analyses reveal that PRR33 regulates cytoskeleton and mitochondrial function. Remarkably, PRR33 interacts with DESMIN, a key regulator of cytoskeleton-mitochondria organization in muscle cells. Abrogation of PRR33 in myocytes substantially abolishes the interaction of DESMIN filaments with mitochondria, leading to abnormal intracellular accumulation of DESMIN and mitochondrial disorganization/dysfunction in myofibers. Together, our findings demonstrate that PRR33 and DESMIN constitute an important regulatory module coordinating mitochondrial organization with muscle differentiation.
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