Kindlin 2 regulates myogenic related factor myogenin via a canonical Wnt signaling in myogenic differentiation.

Bibliographic Details
Title: Kindlin 2 regulates myogenic related factor myogenin via a canonical Wnt signaling in myogenic differentiation.
Authors: Yu Yu, Lihua Qi, Junzhou Wu, Yunling Wang, Weigang Fang, Hongquan Zhang
Source: PLoS ONE, Vol 8, Iss 5, p e63490 (2013)
Publisher Information: Public Library of Science (PLoS), 2013.
Publication Year: 2013
Collection: LCC:Medicine
LCC:Science
Subject Terms: Medicine, Science
More Details: Kindlin 2, as an integrin-associated protein, is required for myocyte elongation and fusion. However, the association of Kindlin 2 with muscle differentiation-related signaling pathways is unknown. Here, we identified a mechanism that Kindlin 2 regulates myogenic regulatory factors myogenin via a canonical Wnt/β-catenin signaling. We found that knockdown of Kindlin 2 leads to the abolishment of β-catenin/TCF4-mediated transcription in C2C12 cells, followed by the impairment of myogenic differentiation. Mechanistically, nuclear translocation of both Kindlin 2 and β-catenin is induced during myogenic differentiation. In particular, Kindlin 2 forms a tripartite complex with active β-catenin and TCF4, and hence co-occupied on the promoter of myogenin to enhance its expression. Functionally, depletion of Kindlin 2 impairs myogenic differentiation via downregulation of myogenin. Taken together, our data reveal that Kindlin 2 is required for Wnt signaling-regulated myogenic differentiation, providing a mechanistic insight into the role of Kindlin-2 in muscle development.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1932-6203
Relation: http://europepmc.org/articles/PMC3661532?pdf=render; https://doaj.org/toc/1932-6203
DOI: 10.1371/journal.pone.0063490
Access URL: https://doaj.org/article/b5d0dc27285f48f6bf0423a011bcfa82
Accession Number: edsdoj.b5d0dc27285f48f6bf0423a011bcfa82
Database: Directory of Open Access Journals
More Details
ISSN:19326203
DOI:10.1371/journal.pone.0063490
Published in:PLoS ONE
Language:English