Testing Suppression in Fer 1 in C

Abstract

For my Spring semester of 2021, I joined Dr. Eric Williams research project on muscular dystrophy. The study we conducted involved C. elegans worms. In the worms, fer-1 is responsible for the fertility of the worms but in humans the gene is responsible for repairing holes in muscle membrane caused by stretching of the muscle. If the fer-1 gene is deemed defective, the worms will become infertile due to defects in sperm. If the human ortholog gene is inactive, muscular dystrophy is the result. One hypothesis is that if we rescue fer-1 defects in the worms, we may be able to do the same in humans. Recent studies suggest that C.elegans fer-1 is also located in the muscle. To test if fer-1 affects muscles, we performed muscle function assays. The hypothesis in the assay is if the fer-1 mutant worms are resistant to paralysis, the muscles are affected. To start the experiment, 3 groups of different worms were grown synchronously to keep differences such as age at a minimum. The 3 worms used were N2 wild type worms, fer-1 mutant worms, and unc-29 worms. The worms were then placed into levamisole dishes with food.N2 wildtype worms are not expected to move in levamisole and unc-29 worms are able to move in levamisole, making N2 our negative control group and unc-29 our positive control group. Fer-1 mutants are our experimental group.

Bryan Bidleman | Biology and Chemistry | Faculty Sponsor Eric Williams