Date of Award

1-2025

Document Type

Thesis

Degree Name

Master of Science (MS)

College/School

College of Science and Mathematics

Department/Program

Biology

Thesis Sponsor/Dissertation Chair/Project Chair

Christos Suriano

Committee Member

Elena Petroff

Committee Member

Carlos Molina

Abstract

Animals face the risk of encountering pathogenic microbes while searching for nutritive resources. Assessing the interplay between the benefits of nutrition vs. the risk of infection might influence the behavioral regulation of immune processes. In Caenorhabditis elegans (C. elegans), a nematode roundworm, behavioral immunity is partially regulated by the innate immune molecule TOL-1: a homolog of vertebrate Toll-like Receptor (TLR) proteins. TOL-1 influences C. elegans pathogen avoidance behaviors by promoting the development of CO2-detecting chemosensory neurons, which detect a signal linked to the presence of harmful pathogens. While TOL-1′s role in pathogen avoidance is well established, its impact in an opposing behavior – foraging – has not yet been explored. In addition to pathogenic bacteria, Escherichia coli (E. coli), preferred food for C. elegans, produces significant levels of CO2 which may inhibit feeding behaviors in a tol-1-dependent manner. We have found that TOL-1, in addition to its contribution to antibacterial immunity, regulates foraging signals by signaling in neurons through the p38 MAPK pathway, especially the PMK-1 protein, to promote turning behavior and limit foraging. When food is scarce, the anorectic TOL-1/PMK-1 pathway is attenuated to promote foraging. These data reveal the integration of TOL-1-mediated immune signaling with behavioral responses to environmental signals, highlight the dynamic role of a conserved innate immune cascade in neurons during both high and low hunger states and identify mechanisms underlying the neuro-immune control of feeding strategies.

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