Distinct mechanisms underlie H2O2 sensing in C. elegans head and tail

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 12 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 12 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.

Automated summary

Environmental oxidative stress poses a threat to cellular integrity and therefore needs to be avoided by living organisms. However, our understanding of how organisms perceive environmental oxidative stress is limited. In this study, using microfluidics, researchers discovered that the tail phasmid PHA neurons in C. elegans function as oxidative stress sensing neurons, similar to 12 pharyngeal neurons. Interestingly, the two types of neurons displayed different responses to H2O2 and light. The study also identified the receptors GUR-3 and LITE-1 as mediators of H2O2 signaling in the neurons, with the peroxiredoxin PRDX-2 playing an essential role in both.