|Abstract||This project was designed to continue and verify the seminal work done by Mr. Christopher Kim. It attempts to prove the existence, and ultimately identify the relative location, of a particular gene in C. elegans that when mutated codes for protein products resistant to the DEET repellant compound. In the event that a mutant strain of C. elegans is successfully generated and isolated, these worms will positively respond to an attractant (IAA), despite special proximity active DEET compound within the medium. This is the criterion implemented in order to correctly determine if a potential mutagenesis transformation was successful. The goal of this transformation is to essentially knockout (or functionally incapacitate) the region of the genome coding for the phenotypic trait of DEET sensitivity. In order to formulate said mutagenesis, the C. elegans of interest were exposed to ethyl methanesulfonate (EMS). Subsequently, the resulting progeny of the organisms exposed to EMS genetic alterations will be tested for the associated phenotypic manifestations of the mutation (specifically DEET resistance) via the previously expounded upon chemo-taxis bioassay. Each mutant strain was re-assayed multiple times, always in comparison to a control wild-type strain, in order rule out inconclusive negatives and false positives. The results of all the subsequent assays were synthesized in order to accurately determine the effectiveness of the mutagenesis by EMS upon a given potentially mutant strain. Following re-affirmation of the mutants isolated by Mr. Kim, 3-factor cross with two phenotypically distinguishable markers were used to map out the specific location of the gene der-1. The der-1 gene is the genetic region hypothesized that when mutated, confers resistance to the repellant powers of DEET. The recombinants prepared were subject to multiple levels of DEET testing for each of the 13 strains in order to determine if DEET resistance in Der-1 is inked or unlinked. If all of the recombinant strains come back unanimously DEET resistant then one could infer that the Der-1 region is indeed unlinked. Furthermore, if the mutant strains tested for in the third and final stage of the experimentation process ends up being uniformly resistant, then that is further affirmation that the Der-1 region is linked. Once several 3-factor crosses have been completed with multiple mutant candidates and DEET resistance is still accounted for in the progeny from the crosses, the candidates will hopefully be sent to the Rockefeller Institute in New York to have their DNA sequenced. Further analysis of the mutants could potentially elucidate the specific mechanism of DEET upon the phenotype of C. elegans that has so eluded researchers. The ultimate goal underlying this research is to accumulate enough data to establish a cornerstone for constructing more efficient commercial insect repellents.