Glutamate signaling mediates C. elegans behavioral plasticity to pathogens

Chun Ying Yu, Howard C. Chang

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

In Caenorhabditis elegans, sensory neurons mediate behavioral response to pathogens. However, how C. elegans intergrades these sensory signals via downstream neuronal and molecular networks remains largely unknown. Here, we report that glutamate transmission mediates behavioral plasticity to Pseudomonas aeruginosa. Deletion in VGLUT/eat-4 renders the mutant animals unable to elicit either an attractive or an aversive preference to a lawn of P. aeruginosa. AMPA-type glutamate receptor GLR-1 promotes the avoidance response to P. aeruginosa. SOD-1 acts downstream of GLR-1 in the cholinergic motor neurons. SOD-1 forms a punctate structure and is localized next to GLR-1 at the ventral nerve cord. Finally, single-copy ALS-causative sod-1 point mutation acts as a loss-of-function allele in both pathogen avoidance and glr-1 dependent phenotypes. Our data showed a link between glutamate signaling and redox homeostasis in C. elegans pathogen response and may provide potential insights into the pathology triggered by oxidative stress in the nervous system.

Original languageEnglish (US)
Article number103919
JournaliScience
Volume25
Issue number3
DOIs
StatePublished - Mar 18 2022
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • General

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