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 show that the tail phasmid PHA neurons function as oxidative stress sensing neurons in C. elegans, and act in a complementary manner to I2 pharyngeal neurons: both can detect H2O2, but with different sensitivities; and both are light sensing, but with distinct responses. We uncovered that while different but related receptors, GUR-3 and LITE-1, mediate H2O2 signaling in I2 and PHA neurons, the peroxiredoxin PRDX-2 is essential in both and may promote H2O2-mediated receptor activation. Altogether, our data suggest that oxidative stress sensing relies on the integration of inputs from head and tail neurons which use partially distinct H2O2 signaling pathways. We propose that this might broaden the sensory repertoire of the nematode to respond appropriately to a large range of oxidative stressors.
Competing Interest Statement
The authors have declared no competing interest.
