Title

Using the Model Organism Caenorhabditis elegans to Study the Role of Epidermal Growth Factor Signaling in Lipid Synthesis

Abstract

Obesity affects more than one-third of adults in the United States. In order to better treat this disease we need to understand how fat synthesis is controlled. I used the model organism Caenorhabditis elegans to study the control of lipid synthesis and in particular LET-23, an epidermal growth factor (EGF) receptor involved in multiple developmental processes. We study the role of LET-23 in lipid synthesis because LET-23 gain of function mutants appear paler than wildtype animals suggesting they have less fat. My research questions were: does LET-23 over activation reduce fat levels and, if so, is it via increasing phosphatidylcholine levels? I found that overactivation of LET-23 decreases fat levels but that underactivation of LET-23 had no effect. I also found that decreasing phosphatidylcholine levels in a LET-23 gain of function background restored fat levels to normal. This suggests that LET-23 overactivation maintains elevated phosphatidylcholine levels to suppress fat synthesis.

Faculty Sponsor

Matthew Crook

Sponsor Department/Programs

Biology

Tracks

Poster Session

Location

Cordiner Hall

Presentation Type

Poster

Research Funding Source or OCS Program

Perry Summer Research Award

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Using the Model Organism Caenorhabditis elegans to Study the Role of Epidermal Growth Factor Signaling in Lipid Synthesis

Cordiner Hall

Obesity affects more than one-third of adults in the United States. In order to better treat this disease we need to understand how fat synthesis is controlled. I used the model organism Caenorhabditis elegans to study the control of lipid synthesis and in particular LET-23, an epidermal growth factor (EGF) receptor involved in multiple developmental processes. We study the role of LET-23 in lipid synthesis because LET-23 gain of function mutants appear paler than wildtype animals suggesting they have less fat. My research questions were: does LET-23 over activation reduce fat levels and, if so, is it via increasing phosphatidylcholine levels? I found that overactivation of LET-23 decreases fat levels but that underactivation of LET-23 had no effect. I also found that decreasing phosphatidylcholine levels in a LET-23 gain of function background restored fat levels to normal. This suggests that LET-23 overactivation maintains elevated phosphatidylcholine levels to suppress fat synthesis.