Taken together, the above results suggest that the ire-1-xbp-1 pathway functions to protect the host against the PFT Cry5B. However, an alternative explanation for our results is that animals mutant in this pathway (e.g., xbp-1 mutant animals) are sickly and have compromised health and therefore would respond poorly to any toxic insult. To address this alternative hypothesis, we tested whether xbp-1(zc12) animals are hypersensitive to two toxic chemical compounds, the heavy metal CuSO 4 (a toxic insult that kills with kinetics similar to Cry5B) and the oxidative stress agent H 2 O 2 (a toxic insult that kills rapidly). The mutant xbp-1(zc12) has the same sensitivity as wild type to killing by either CuSO4 or H 2 O 2 ( Figure 2D and 2E; Table 1 ). These data argue against the supposition that this mutant is hypersensitive to the PFT merely because it is generally unhealthy. Rather, the protective response is somewhat specific against the PFT. These conclusions are strengthened by the finding that C. elegans lacking the UPR respond normally to attack by the pathogenic bacteria Pseudomonas aeruginosa, which does not make a PFT ( Figure 2F and Table 1 ).