By Victoria Ashton, Delaney Baratka, John Conrad Tan

Faculty Mentor: Dr. Ginny Morriss

Abstract

DM1 is a progressive and multi-systemic muscle-wasting disorder caused by an expansion of CTG repeats in the 3’ UTR region in the DMPK gene. Though the mechanism of how DM1 works is still unknown, research has indicated that PDGFRβ pathway signaling is de-regulated in mice and may play a role in DM1. For this experiment, RNAi technology was used to knockdown pvr, the PDGFRβ fly homolog, in Drosophila to confirm if decreased pvr plays a role in DM1. Fly phenotypes were measured using flight and climbing assays, and the relative expression of pvr was calculated using qPCR to examine the efficiency of the knockdown. The expected results should confirm whether decreased pvr plays a role in DM1, and could lead to more effective treatments for the disorder.