FIG. 5.

DCR-1 mediates the H₂O₂-induced inhibition of thermotolerance in C. elegans. Effect of H₂O₂ on intrinsic and acquired thermotolerance in worms fed by empty (EV, A) or dcr-1(RNAi) (B) vectors, respectively. Treatments were as in Figure 4. Note that the activatory effect of preconditioning heat shock was less pronounced on RNAi plates. In EV-fed worms (A) only heat shock, while in dcr-1(RNAi)-fed worms (B) both heat shock as well as H₂O₂+heat shock induced a significantly higher survival compared with controls (p<0.001). (C) Both heat shock and H₂O₂+heat shock induces a significant increase in thermotolerance in dcr-1(ok247);unc-32(e189) nematodes (p<0.0001 vs. control). Survival curves are representatives of three experiments yielding similar results. (D) H₂O₂ does not compromise RNA interference. Epifluorescence image demonstrating increased expression of pajm::GFP (harboring an anti-GFP hairpin siRNA in addition to the GFP sequence) in the GR1401 RNA interference reporter strain fed by dcr-1(RNAi). Arrows point to specific dots localized to epithelial seam cells. In contrast, H₂O₂ (100 μM for 1 h) treatment followed by a 12- or 24-h recovery did not inhibit GFP silencing. Please note the autoflurescence of oxidatively stressed worms. Representative image from three independent experiments. (To see this illustration in color the reader is referred to the web version of this article at www.liebertonline.com/ars).