Date of Submission

Spring 2013

Academic Program


Project Advisor 1

Michael Tibbetts

Project Advisor 2

Heeun Jang

Abstract/Artist's Statement

Social feeding/foraging/aggregation behavior in Caenorhabditis elegans is a simple system for studying neural circuitry and molecular players that regulate a complex behavior. npr-1 and daf-7 pathways regulate the social feeding behavior in parallel in response to various sensory cues such as noxious stimuli, population density, food availability, oxygen level and pheromones. Here the role of pdk-1, a candidate gene identified from a mutagenesis screen performed to isolate molecular players responsible for aggregation behavior in C. elegans, was investigated in contributing to the social feeding behavior in the worms. The candidacy for causal mutation was examined by creating transgenic lines carrying extrachromosal array with GFP marker that contained genomic fragment of wildtype pdk-1 gene under the endogenous promoter, gut promoter (elt-2) or pan-neuronal promoter (h20). A fluorescence microscope setup for a normal dissecting scope was also constructed to sort out GFP positive worms. After assaying the transgenic lines for aggregation phenotype, we concluded that wildtype pdk-1 gene rescued the phenotype and mutation in pdk-1 is the causal mutation in both of our mutant lines.

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