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 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. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=113 SRC="FIGDIR/small/451501v1_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@5901a8org.highwire.dtl.DTLVardef@17bbfd9org.highwire.dtl.DTLVardef@1705f18org.highwire.dtl.DTLVardef@732478_HPS_FORMAT_FIGEXP M_FIG C_FIG