College Honors Program

Title

Investigating the Roles of the Spinal Muscular Atrophy (SMA) Genes smn-1 and mog-4 in the Insulin-Signaling Response to a High-Glucose Diet

Date of Creation

5-31-2023

Document Type

Campus Access Only

Department

Biology

First Advisor

Michelle A. Mondoux

Abstract

Spinal muscular atrophy (SMA) is a human neurodegenerative disease caused by a mutation to the SMN-1 gene. Our lab identified the C. elegans homolog smn-1 and its interactor mog-4 as glucose-specific insulin-signaling regulators. Because the insulin-signaling pathway is conserved between humans and C. elegans, we can model the relationship between these genes and this pathway. Increased insulin signaling in the presence of glucose decreases healthspan (healthy life period) and lifespan in C. elegans. We can use C. elegans daf-2 insulin receptor mutants to model low insulin-signaling levels. In this study, I predicted that decreased insulin signaling due to knockdowns of smn-1 and mog-4 would result in increased healthspan and lifespan. Using daf-2(e1368) and daf-2(e1370) mutant strains, I assessed the effects of these knockdowns. I found that mog-4 knockdown decreases the severity of the healthspan decline in aged daf-2(e1368) worms on a high-glucose diet, but not in daf-2(e1370). mog-4 knockdown does not extend lifespan on a high-glucose diet in either mutant. smn-1 does not increase healthspan or lifespan in daf-2(e1370) worms on a high-glucose diet. These results suggest that when insulin signaling is low, mog-4 only regulates healthspan while smn-1 does not regulate healthspan or lifespan.

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