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Research Article
1PVLSI 2University of Massachusetts
Submitted 27 August 2009 ; revised 23 October 2009 ; accepted in final form 3 November 2009
Acheron (Achn) was originally identified as novel gene that is induced when insect muscles become committed to die at the end of metamorphosis. In separate studies, we have demonstrated that Achn acts upstream of MyoD and is required by mammalian myoblasts to either differentiate or undergo apoptosis following loss of growth factors. In the present study we examined the role of Achn in regulating integrin-extracellular matrix (ECM) interactions that are required for myogenesis. Both control C2C12 myoblasts, and those engineered to express ectopic Achn, expressed the fibronectin receptor integrin
5β1 in the presence of growth factors and the laminin receptor
7β1 following growth factor withdrawal. Expression of the laminin receptor was blocked in cells expressing either Achn antisense or an Achn deletion mutant that blocks differentiation. Control cells and those expressing ectopic Achn undergo sequential and transient increases in both substrate adhesion and migration prior to cell fusion. Blockade of Achn expression reduced these effects on laminin but not on fibronectin. Taken together, these data suggest that Achn may influence differentiation in part via its control of cell adhesion dynamics.
C2C12; differentiation; satellite cell; integrin signaling
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