Muscle cells must anchor to their environment, the extracellular matrix (ECM), in order to function properly. Muscular dystrophy occurs when muscle cells cannot anchor to the ECM because specific protein complexes, such as the dystroglycan complex, are disrupted. Previously published studies have shown that overexpressing Paxillin can reduce dystrophy in dag1 deficient embryos. The aim of this study is to determine which domains of Paxillin are necessary to rescue dystrophy by overexpressing Paxillin with the LD2 or LD4 domains knocked out in dystrophic embryos. However, disruption of Dag1 via the previous method stopped producing the muscular dystrophy phenotype, so ethanol (EtOH) treatment was used to induce dystrophy. It was determined that this is not a sufficient method of inducing dystrophy for this study. The EtOH treatment was inconsistent, and Paxillin overexpression was unable to rescue dystrophy in EtOH treated zebrafish. Furthermore, the dystrophy seen in EtOH treated embryos was much more severe than that seen in typical muscular dystrophy. Although this experiment could not be used to determine the necessity of the LD domains of Paxillin, it did give insight into the toxicity of EtOH. This information will be useful as we move on using different techniques.
Pasquarella, Margaret E., "Exploring the Mechanisms Involved in Paxillin Amerlioration of Dystrophies in Zebrafish" (2016). Honors College. 411.