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Vidal-Gadea Lab
Vidal-Gadea Lab
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​Duchenne Muscular Dystrophy​ (DMD) is a genetic disorder affecting 1 in 3,500 male births. It is caused by a mutation in the dystrophin gene, one of the longest genes in the human genome. Dystrophin is involved in the transmission of the force generated during muscle activity. Defective dystrophin proteins lead to muscle damage and failure. The nematode C. elegans uses dystrophin in much the same way humans do. As such, these tiny worms afford us the opportunity to study DMD with the unparalleled experimental ease associated with the study of these organisms.

​Our lab has developed several burrowing assays to challenge motor output in dystrophic animals. Mutants mimicking Duchenne muscular dystrophy by lacking a functional ortholog of the dystrophin protein, DYS-1, crawl normally but are severely impaired in burrowing. Muscular degeneration in the dys-1 mutant is hastened and exacerbated by burrowing, while wild type shows no such damage (figure). Our students performed a genetic screen using dys-1 worms and isolated several suppressor with proficient burrowing despite their dys-1 mutant background. 

In our lab, work on muscular dystrophy focuses on several goals:

1)  Identifying the molecular mechanisms by which muscles become impaired during the progression of DMD.
2) Identifying the mutations responsible for the rescue of the dys-1 phenotype observed in suppressor mutants
3) Identifying novel and conserved molecular targets that may contribute to the alleviation of DMD symptoms.

A dedicated team of researchers in our lab are working to improve the quality of life of individuals strugling with this terrible disease.

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Kiley Hughes (PhD), Monica Tamrazi (MS), and Dana Niswonger (MS) are our graduate team working on the Duchenne muscular dystrophy.