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Updated: May 13, 2025

Studying Wnt Signaling During Patterning of Conducting Airways
Published on: October 16, 2016
RNF138 regulates skeletal muscle differentiation via the Wnt/β-catenin signaling pathway
Wenhao Wang1, Zhuohua Wang1, Rourong Li1
1The Molecular Cancer Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, No. 66, Gongchang Road, Guangming District, Shenzhen, Guangdong 518107, China.
Abstract:
Rationale: Myogenesis is a strictly regulated process driven by signaling pathways activating muscle-specific gene expression. During myogenesis, muscle stem cells exhibit DNA damage response (DDR) features, which are essential for myoblast differentiation and skeletal muscle regeneration. However, the specific roles of DDR-associated proteins in these processes are not yet fully understood. Methods: Gene knockdown and knockout were used in cell and animal models to study RNF138's function in myoblast differentiation and skeletal muscle regeneration. Multi-omics profiling, including transcriptomics and proteomics, was conducted to identify the key proteins regulated by RNF138 in myogenesis. Protein turnover assays were utilized to investigate RNF138's role in APC protein turnover. Immunofluorescence microscopy was performed to confirm the protein colocalization and subcellular localization. Results: RNF138 expression increases during myoblast differentiation and in regenerating myofibers following muscle injury. Knockdown of RNF138 in C2C12 myoblasts impairs myogenic differentiation and fusion. Additionally, Rnf138-deficient mice exhibit delayed muscle regeneration following cardiotoxin-induced injury. Multi-omics profiling, including transcriptomics and proteomics, reveals that Wnt/β-catenin signaling, a key driver of myogenic differentiation, is enhanced by RNF138. Mechanistically, RNF138 stabilizes β-catenin and enhances its nuclear localization by facilitating lysosomal degradation of APC, a component of the β-catenin degradation complex responsible for mediating the export of β-catenin from the nucleus to the cytoplasm for further ubiquitin-proteasome degradation. Conclusions: We reveal a noncanonical role for RNF138, an E3 ubiquitin ligase, as a positive regulator of myoblast differentiation and skeletal muscle regeneration via the Wnt/β-catenin pathway. This finding highlights the noncanonical function of RNF138 beyond its known roles in DDR and other cellular processes. Therefore, RNF138 provides a potential link between DDR and myoblast differentiation, offering new insights into the molecular regulation of muscle regeneration.
Insights
RNF138 promotes muscle stem cell differentiation and regeneration by stabilizing beta-catenin via the Wnt/beta-catenin pathway. This reveals a new role for RNF138 beyond DNA damage response in muscle repair.
Area of Science:
- Muscle biology
- Cellular signaling
- Regenerative medicine
Background:
- Myogenesis requires precise regulation of gene expression by signaling pathways.
- Muscle stem cells utilize DNA damage response (DDR) features for differentiation and regeneration.
- The precise roles of DDR proteins in myogenesis are not fully understood.
Purpose of the Study:
- To investigate the function of RNF138 in myoblast differentiation and skeletal muscle regeneration.
- To elucidate the molecular mechanisms by which RNF138 regulates myogenesis.
- To explore the link between DDR and muscle regeneration.
Main Methods:
- Gene knockdown and knockout in cell and animal models.
- Multi-omics profiling (transcriptomics, proteomics).
- Protein turnover assays and immunofluorescence microscopy.
Main Results:
- RNF138 expression is upregulated during myoblast differentiation and muscle regeneration.
- RNF138 deficiency impairs myoblast differentiation, fusion, and delays muscle regeneration in mice.
- RNF138 enhances Wnt/β-catenin signaling by stabilizing β-catenin and promoting its nuclear localization through APC degradation.
Conclusions:
- RNF138, an E3 ubiquitin ligase, positively regulates myoblast differentiation and muscle regeneration.
- RNF138 acts via the Wnt/β-catenin pathway, stabilizing β-catenin.
- This study uncovers a noncanonical function of RNF138, linking DDR to muscle regeneration.
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