Entomopathogenic nematodes (EPNs) are insect-killing parasitic worms that are utilized in agriculture and home-garden use against a variety of insect pests. It is the infective juvenile stage (IJ) of the EPN life cycle responsible for locating, infecting and colonizing a new insect host to continue the life cycle and produce progeny. My research revealed that EPN species within the genus Steinernema, responded to host volatiles, in species—specific patterns with regard to both behavioral trends to the progression of infection, as well as overall participation. Analysis of host-odor profiles- for both naive and infected hosts (including recently infected and long-term, resource depleted insect cadavers) produced a variety of odors and one of the more notable odors produced was 3-methyl-2-buten-1-ol (prenol). EPN IJs were found to be repelled by prenol at a variety of doses (ranging from 2M to 20mM) and prenol yielded age-dependent increases in dispersal, implicating prenol as a potential IJ dispersal cue. However, lack of molecular tools in EPNs prevented investigations into the molecular underpinnings of how prenol is detected and translated into the observable repulsion. To overcome this obstacle, we leveraged the model organisms: Caenorhabditis elegans which exhibits attraction to prenol. Through use of natural variation, genome-wide association, and leveraging multiple genetic resources in the C. elegans community we identified the involvement of the AWC neuron in detection and response to prenol as well as eight genes that influence responses to prenol, including genes that have not previously been shown to affect chemotactic behaviors: dod-17, clec-39, dcap-1 and dcap-2. For many of these genes, we have found EPN orthologs exist, meaning we have uncovered information that potentially could be utilized to better understand EPN behavioral ecology such that EPNs may be improved or utilized more effectively in the future.