Adapting cytoskeleton-mitochondria patterning with myocyte differentiation by promyogenic PRR33.

IF 13.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Cell Death and Differentiation Pub Date : 2024-08-15 DOI:10.1038/s41418-024-01363-w
Xuyang Fu, Feng Zhang, Xiaoxuan Dong, Linbin Pu, Yan Feng, Yang Xu, Feng Gao, Tian Liang, Jianmeng Kang, Hongke Sun, Tingting Hong, Yunxia Liu, Hongmei Zhou, Jun Jiang, Deling Yin, Xinyang Hu, Da-Zhi Wang, Jian Ding, Jinghai Chen
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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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通过原发性 PRR33 使细胞骨架-微粒体模式化与肌细胞分化相适应
肌肉生成过程中协调的细胞骨架-软骨组织对肌肉的发育和功能至关重要。我们对其潜在调控机制的了解仍然不足。在这里,我们发现了一种新的肌肉富集蛋白--PRR33,它在肌肉生成过程中上调并充当原肌纤维生成因子。在 C2C12 中缺失 Prr33 会抑制成肌细胞分化。小鼠基因缺失 Prr33 会缩小肌纤维尺寸并降低肌肉强度。Prr33 突变体小鼠还表现出肌生成障碍和肌肉损伤再生缺陷。相互作用组和转录组分析表明,PRR33 调节细胞骨架和线粒体功能。值得注意的是,PRR33 与 DESMIN 相互作用,DESMIN 是肌肉细胞中细胞骨架-线粒体组织的关键调节因子。在肌细胞中减弱 PRR33 会大大降低 DESMIN 细丝与线粒体的相互作用,从而导致 DESMIN 在细胞内的异常积聚以及肌纤维中线粒体的紊乱/功能障碍。我们的研究结果表明,PRR33 和 DESMIN 构成了协调线粒体组织和肌肉分化的重要调控模块。
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来源期刊
Cell Death and Differentiation
Cell Death and Differentiation 生物-生化与分子生物学
CiteScore
24.70
自引率
1.60%
发文量
181
审稿时长
3 months
期刊介绍: Mission, vision and values of Cell Death & Differentiation: To devote itself to scientific excellence in the field of cell biology, molecular biology, and biochemistry of cell death and disease. To provide a unified forum for scientists and clinical researchers It is committed to the rapid publication of high quality original papers relating to these subjects, together with topical, usually solicited, reviews, meeting reports, editorial correspondence and occasional commentaries on controversial and scientifically informative issues.
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