Immune Toll-like Receptor Signaling Modulates C.elegans Feeding Behavior
Presentation Type
Poster
Faculty Advisor
Christos Suriano
Access Type
Event
Start Date
26-4-2024 12:45 PM
End Date
26-4-2024 1:44 PM
Description
Animals face the risk of encountering pathogenic microbes while foraging for resources. Assessing the risk of nutrition vs. infection can result in the behavioral regulation of immune processes. Behavioral immunity in the nematode roundworm Caenorhabditis elegans (C. elegans) is regulated by the innate immune molecule TOL-1: a homolog of vertebrate Toll-like Receptor (TLR) proteins that influences C. elegans pathogen avoidance behaviors by promoting the development of CO2-detecting chemosensory neurons. While TOL-1’s role in pathogen avoidance is well established, its role in an opposing behavior – foraging – has not been examined. In addition to pathogenic bacteria, preferred food for C. elegans, such as Escherichia coli (E. coli), create significant environmental CO2 levels which may limit feeding behaviors in a tol-1 dependent manner. We have found that in addition to conferring antibacterial immunity, TOL-1 signals through the p38 MAPK homolog, PMK-1, to limit foraging when food is abundant and that the TOL-1;PMK-1 pathway is attenuated during high hunger states to promote foraging. These data highlight the role of a conserved innate immune cascade, TOL-1 and its signaling partners, in modulating risk aversion during both high and low hunger states and demonstrate the importance of neuro-immune signaling in the generation of complex foraging behavior.
Immune Toll-like Receptor Signaling Modulates C.elegans Feeding Behavior
Animals face the risk of encountering pathogenic microbes while foraging for resources. Assessing the risk of nutrition vs. infection can result in the behavioral regulation of immune processes. Behavioral immunity in the nematode roundworm Caenorhabditis elegans (C. elegans) is regulated by the innate immune molecule TOL-1: a homolog of vertebrate Toll-like Receptor (TLR) proteins that influences C. elegans pathogen avoidance behaviors by promoting the development of CO2-detecting chemosensory neurons. While TOL-1’s role in pathogen avoidance is well established, its role in an opposing behavior – foraging – has not been examined. In addition to pathogenic bacteria, preferred food for C. elegans, such as Escherichia coli (E. coli), create significant environmental CO2 levels which may limit feeding behaviors in a tol-1 dependent manner. We have found that in addition to conferring antibacterial immunity, TOL-1 signals through the p38 MAPK homolog, PMK-1, to limit foraging when food is abundant and that the TOL-1;PMK-1 pathway is attenuated during high hunger states to promote foraging. These data highlight the role of a conserved innate immune cascade, TOL-1 and its signaling partners, in modulating risk aversion during both high and low hunger states and demonstrate the importance of neuro-immune signaling in the generation of complex foraging behavior.
Comments
Additional Authors: Malak Saleh, Emily Kopecky, Cindy Mutafoglu, Retwika Ganguly