By Carleigh Wood

Faculty Mentor: Dr. Ginny Morriss

Abstract

This research investigated how increasing Iditarod (Idit), the Drosophila melanogaster homolog of irisin, affects the progression of Myotonic Dystrophy type 1 (DM1). DM1 is caused by an expansion of CTG repeats in the DMPK gene, which leads to muscle weakening and wasting. Given irisin’s role in promoting muscle hypertrophy and its potential therapeutic effects in muscular dystrophies, this study explored how activity-induced Idit expression might impact muscle structure and function in DM1 model flies. Healthy control (CTG20) and DM1 (CTG250) flies were generated using classical genetics. Both groups underwent a three-week exercise regimen on a PowerTower, designed to induce Idit expression through physical activity. Muscle function was assessed by measuring climbing and flight muscle performance. It was predicted that exercised flies would exhibit improved muscle function, while sedentary flies would display more severe DM1-related impairments. Genetic overexpression and RT-qPCR validation were begun, but not yet successfully completed. This study provides early indications that exercise may mitigate DM1-related muscle degeneration and highlights the potential of myokines like irisin as therapeutic targets in muscular dystrophies.