The role of immune molecules in foraging behavior: Tol-1 inhibits C. elegans foraging behavior in a feeding state dependent manner
Presentation Type
Poster
Faculty Advisor
Christos Suriano
Access Type
Event
Start Date
26-4-2023 9:45 AM
End Date
26-4-2023 10:44 AM
Description
Animals face the risk of encountering pathogenic microbes while foraging for resources. Assessing the risk of resources vs. infection can result in the behavioral regulation of immune processes. Behavioral immunity in C. elegans is regulated in part by Tol-1: a homolog of vertebrate Toll-like Receptor (TLR) proteins that is involved in both C. elegans innate immunity and the generation of pathogen avoidance behaviors. C. elegans can detect increased environmental CO2 levels, a proxy for pathogenic microbial metabolism and generate aversive behaviors in a Tol-1 dependent manner. While Tol-1’s role in pathogen avoidance is well established, its role in an opposing behavior – foraging – has not been examined. Preferred food for C. elegans, such as E. coli, create similar environmental CO2 levels to pathogenic bacteria, which may limit foraging behaviors in a Tol-1 dependent manner. We have found that animals with a deletion of the Toll/Interleukin Receptor Binding Domain (TIR BD) of Tol-1 are significantly more likely to engage in foraging behaviors than wildtype counterparts in a hunger state dependent manner indicating that Tol-1 limits foraging behaviors when food is abundant. Additionally, increased foraging in both TIR BD KO and starved wild-type animals is associated with the altered expression of genes homologous to those involved in vertebrate TLR9 signaling. These data demonstrate the importance of neuro-immune interactions and hunger state in the generation of foraging behaviors.
The role of immune molecules in foraging behavior: Tol-1 inhibits C. elegans foraging behavior in a feeding state dependent manner
Animals face the risk of encountering pathogenic microbes while foraging for resources. Assessing the risk of resources vs. infection can result in the behavioral regulation of immune processes. Behavioral immunity in C. elegans is regulated in part by Tol-1: a homolog of vertebrate Toll-like Receptor (TLR) proteins that is involved in both C. elegans innate immunity and the generation of pathogen avoidance behaviors. C. elegans can detect increased environmental CO2 levels, a proxy for pathogenic microbial metabolism and generate aversive behaviors in a Tol-1 dependent manner. While Tol-1’s role in pathogen avoidance is well established, its role in an opposing behavior – foraging – has not been examined. Preferred food for C. elegans, such as E. coli, create similar environmental CO2 levels to pathogenic bacteria, which may limit foraging behaviors in a Tol-1 dependent manner. We have found that animals with a deletion of the Toll/Interleukin Receptor Binding Domain (TIR BD) of Tol-1 are significantly more likely to engage in foraging behaviors than wildtype counterparts in a hunger state dependent manner indicating that Tol-1 limits foraging behaviors when food is abundant. Additionally, increased foraging in both TIR BD KO and starved wild-type animals is associated with the altered expression of genes homologous to those involved in vertebrate TLR9 signaling. These data demonstrate the importance of neuro-immune interactions and hunger state in the generation of foraging behaviors.