Abstract
Environmental oxidative stress threatens cellular integrity and should therefore be avoided by living organisms. Yet, relatively little is known about environmental oxidative stress perception. Here, using microfluidics, we showed that like I2 pharyngeal neurons, the tail phasmid PHA neurons function as oxidative stress sensing neurons in C. elegans, but display different responses to H2O2 and light. We uncovered that different but related receptors, GUR-3 and LITE-1, mediate H2O2 signaling in I2 and PHA neurons. Still, the peroxiredoxin PRDX-2 is essential for both, and might promote H2O2-mediated receptor activation. Our work demonstrates that C. elegans can sense a broad range of oxidative stressors using partially distinct H2O2 signaling pathways in head and tail sensillae, and paves the way for further understanding of how the integration of these inputs translates into the appropriate behavior.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
This revised version includes more data (sek-1/MAPKK mutant analyses), which strengthened our conclusion that the p38MAPK pathway is required in PHA neurons for sensitivity to low doses of H2O2. In addtition, we re-did all statistical analyses, taking into account the multiple comparisons problem. Importantly, performing these more stringent statistical analyses did not change our conclusions. All figures have been updated, and supplementary material includes 4 new movies and 2 new figures.
