Lack of galectin-1 results in defects in myoblast fusion and muscle regeneration
Article first published online: 15 MAR 2007
Copyright © 2007 Wiley-Liss, Inc.
Volume 236, Issue 4, pages 1014–1024, April 2007
How to Cite
Georgiadis, V., Stewart, H. J.S., Pollard, H. J., Tavsanoglu, Y., Prasad, R., Horwood, J., Deltour, L., Goldring, K., Poirier, F. and Lawrence-Watt, D. J. (2007), Lack of galectin-1 results in defects in myoblast fusion and muscle regeneration. Dev. Dyn., 236: 1014–1024. doi: 10.1002/dvdy.21123
- Issue published online: 15 MAR 2007
- Article first published online: 15 MAR 2007
- Manuscript Accepted: 14 FEB 2007
- Muscular Dystrophy Campaign, UK. Grant Number: RA3/648
- Anatomical Society Great Britain and Ireland
- Association Francaise Contre les Myopathies. Grant Number: DD/NM/2003/2563/9735
- myoblast fusion;
- muscle regeneration
Galectin-1 has been implicated in the development of skeletal muscle, being maximally expressed at the time of myofiber formation. Furthermore, in the presence of exogenous galectin-1, mononuclear myoblasts show increased fusion in vitro. In the current study, we have used the galectin-1 null mouse to elucidate the role of galectin-1 in skeletal muscle development and regeneration. Myoblasts derived from the galectin-1 mutant showed a reduced ability to fuse in vitro. In galectin-1 null mutants, there was evidence of a delay in muscle fiber development at the neonatal stage and muscle fiber diameter was reduced when compared with wild-type at the adult stage. Muscle regeneration was also compromised in the galectin-1 mutant with the process being delayed and a reduced fiber size being maintained. These results, therefore, show a definitive role for galectin-1 in fusion of myoblasts both in vitro, in vivo, and in regeneration after recovery from induced injury. Developmental Dynamics 236:1014–1024, 2007. © 2007 Wiley-Liss, Inc.