ArticleFrontiers in cell and developmental biology2026
Planar cell polarity protein Vangl2 interacts with M-cadherin and stabilizes its cell surface expression in mouse C2C12 myoblasts.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Skeletal muscle regeneration depends on muscle stem cells (MuSCs), in which cadherin-mediated adhesion and planar cell polarity (PCP) signaling play critical roles. M-Cadherin is the major cadherin expressed in MuSCs; however, its functional link to PCP proteins remains unclear. In this study, we demonstrate that the PCP core component Vangl2 co-localizes with M-cadherin at the MuSC-myofiber boundary and directly interacts with it in C2C12 cells. Mutagenesis analyses revealed that the catenin-binding domain of M-cadherin and the C-terminal domain of Vangl2 are required for this interaction, which uniquely enables M-cadherin to form a ternary complex with Vangl2 and β-catenin. Knockdown of Vangl2 impaired myoblast fusion, reduced the expression of MyoD and Myomixer, and decreased the cell surface stability of M- and N-cadherins, while canonical Wnt/β-catenin and Akt signaling were unaffected. These findings demonstrate that Vangl2 stabilizes cadherins at the plasma membrane and promotes myogenic differentiation, suggesting a previously unrecognized role of PCP signaling in skeletal muscle maintenance and regeneration.
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