Presentation description

Even after decades of biological research, the molecular and genetic mechanisms driving genetically identical organisms to change their phenotype in response to their environment remain surprisingly unclear. This occurrence, known as phenotypic plasticity, is evident in the nematode Pristionchus pacificus, which develops two distinct mouth forms, each regulated by the eud-1 gene. Increased eud-1 expression in environments of overcrowding and starvation leads to a eurystomatous morphology, including a wide mouth and two teeth used for predation on other nematodes. Conversely, in low population density, food-rich environments, eud-1 is expressed at a decreased level, resulting in a stenostomatous morphology categorized by a narrow mouth, one tooth, and a microorganism-based diet. The upstream region of eud-1 plays a significant role in deciphering environmental cues through environmentally influenced transcription factors binding to DNA areas in the region; however, these specific areas in the pathway are unknown. We hypothesize that through evaluation of nematodes with DNA deletions in the upstream region of the eud-1 gene, we can understand the extent to which phenotypic plasticity in nematode mouth morphology is expressed and altered. Our initial results indicate that the right region deletion has the strongest effect on eud-1 gene activity. By maintaining a controlled environment with expected phenotypic outcomes, we can detect how the deletions disrupt morphology. Additionally, qPCR will be used to quantify eud-1 expression in modified nematode strains. Future work includes narrowing deletions to more precise regions. Ultimately, this research aims to deepen our understanding of the genetic mechanisms underlying phenotypic plasticity.