Amyotrophic Lateral Sclerosis (ALS), or Lou Gehrig's disease, is a progressive neurodegenerative disease where motor neurons die back from the neuromuscular junction. Currently, no effective cure exists, so death inevitably follows the symptoms of muscle atrophy and paralysis. Mutations in the gene Cu/Zn Superoxide Dismutase 1 (SOD1) account for about 20% of cases of familial ALS and 3% of sporadic cases. The mechanism of SOD1 toxicity remains to be elucidated. This project explores the molecular mechanisms of disease progression for SOD1-based ALS through protein and RNA analyses of a knock-in model in Drosophila melanogaster. We find that SOD1 levels in the model are comparable to wild type, SOD1 is not present in an insoluble protein fraction, and maternal SOD1 RNA persists in mutant larvae for over 48 hrs.
Bredvik, Kirsten, and Şahin, Asli,
"Characterization of a Knock-in Model of SOD1-mediated ALS in Drosophila melanogaster"
(2015).
Summer Research Symposium.
Brown Digital Repository. Brown University Library.
https://doi.org/10.26300/12hc-s910
Each year, Brown University showcases the research of its undergraduates at the Summer Research Symposium. More than half of the student-researchers are UTRA recipients, while others receive funding from a variety of Brown-administered and national programs and fellowships and go …
