Activation of YAP regulates muscle fiber size in a PKC-dependent mechanism during chick in vitro myogenesis.

IF 1.7 3区生物学 Q4 CELL BIOLOGY

Journal of Muscle Research and Cell Motility Pub Date : 2022-06-01 Epub Date: 2021-08-19 DOI:10.1007/s10974-021-09608-8

Geyse Gomes, Kayo Moreira Bagri, Ivone de Andrade Rosa, Arnon Dias Jurberg, Claudia Mermelstein, Manoel Luis Costa

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引用次数: 3

Abstract

The formation of skeletal muscle fibers is an intricate process controlled by a multitude of signaling pathways, including Wnt, Shh, and FGF. However, the role of the Hippo pathway during vertebrate myofiber formation has conflicting reports, which we decided to address in chick muscle cultures. We found that the transcriptional regulator Yes-associated protein (YAP) was highly concentrated within the nuclei of myoblasts. As cells differentiate into myotubes, YAP localization shifted to the cell cytoplasm in more mature myotubes. Treatment of cultures with XMU-MP-1 (XMU), a MST1/2 inhibitor, stimulated the nuclear localization of YAP in myoblasts and in myotubes, upregulated myogenin, and promoted myoblast fusion, ultimately resulting in the formation of large and fully striated multinucleated myotubes. The XMU-induced phenotype was blocked by the protein kinase C (PKC) inhibitor calphostin, which raises the possibility that the Hippo pathway controls the growth of skeletal muscle fibers through a PKC-dependent mechanism.

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在鸡体外肌肉形成过程中，YAP的激活以pkc依赖的机制调节肌纤维大小。

骨骼肌纤维的形成是一个复杂的过程，受多种信号通路控制，包括Wnt、Shh和FGF。然而，Hippo通路在脊椎动物肌纤维形成过程中的作用有相互矛盾的报道，我们决定在鸡肌肉培养中解决这个问题。我们发现转录调控因子Yes-associated protein (YAP)在成肌细胞细胞核内高度集中。当细胞分化为肌管时，YAP定位在更成熟的肌管中转移到细胞质中。用MST1/2抑制剂XMU- mp -1 (XMU)处理培养物，刺激成肌细胞和肌管中YAP的核定位，上调肌原素，促进成肌细胞融合，最终形成大且完全条纹的多核肌管。xmu诱导的表型被蛋白激酶C (PKC)抑制剂calphostin阻断，这提出了Hippo通路通过PKC依赖机制控制骨骼肌纤维生长的可能性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Muscle Research and Cell Motility 生物-细胞生物学

CiteScore

6.20

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.