Muscular degeneration in the absence of dystrophin is a calcium-dependent process

Duchenne muscular dystrophy (DMD) is a progressive degenerative muscular di sease that is due to mutations in the dystrophin gene [1]. Neither the func tion of dystrophin nor the physiopathology of the disease have been clearly established yet. Several groups have reported elevated calcium concentrati ons in the mdx mouse model of DMD, but the effect of calcium levels on the progression of the disease continues to be a matter of debate [2-4]. Here, we show that, in Caenorhabditis elegans, a gain-of-function mutation in the egl-19 calcium channel gene dramatically increases muscle degeneration in dystrophin mutants. Conversely, RNAi-mediated inhibition of egl-19 function reduces muscle degeneration by half. Therefore, our results demonstrate th at calcium channel activity is a critical factor in the progression of dyst rophin-dependent muscle degeneration.