Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
BMC Cell Biol. 2008 Jul 8;9:36. doi: 10.1186/1471-2121-9-36.

Kindlin-2 is required for myocyte elongation and is essential for myogenesis.

Author information

  • 1Department of Pediatrics, University of Michigan, Ann Arbor, USA. jamedowl@umich.edu

Abstract

BACKGROUND:

Integrins are required for normal muscle differentiation and disruptions in integrin signaling result in human muscle disease. The intracellular components that regulate integrin function during myogenesis are poorly understood. Unc-112 is an integrin-associated protein required for muscle development in C. elegans. To better understand the intracellular effectors of integrin signaling in muscle, we examined the mammalian homolog of Unc-112, kindlin-2.

RESULTS:

Kindlin-2 expression is upregulated during differentiation and highly enriched at sites of integrin localization. RNAi knockdown of kindlin-2 in C2C12 cells results in significant abnormalities during the early stages of myogenesis. Specifically, differentiating myocytes lacking kindlin-2 are unable to elongate and fail to fuse into multinucleated myotubes. These changes are correlated with decreased cell substratum adhesion and increased cell motility. They are also associated with redistribution of a known kindlin-2 binding partner, integrin linked kinase (ILK), to the membrane insoluble subcellular fraction.

CONCLUSION:

In all, our study reveals kindlin-2 as a novel integrin adaptor protein important for muscle differentiation, and identifies it particularly as a critical regulator of myocyte elongation.

PMID:
18611274
[PubMed - indexed for MEDLINE]
PMCID:
PMC2478659
Free PMC Article

Images from this publication.See all images (10)Free text

Figure 1
Figure 2
Figure 3
Figure 6
Figure 4
Figure 5
Figure 7
Figure 8
Figure 9
Figure 10
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for BioMed Central Icon for PubMed Central
    Loading ...
    Write to the Help Desk