To determine whether the ER stress response played a role in the defense of C. elegans against the PFT, C. elegans mutants in the ER stress response pathway were qualitatively compared to wildtype N2 animals in their susceptibilities to Cry5B. The mutants that were tested included those encoding the three ER stress transducer genes, atf-6(ok551), pek-1(ok275), and ire-1(v33), as well as xbp-1(zc12); these mutations are predicted or known to be loss of function mutations in their respective genes [11, 12, 13] . In the absence of Cry5B, the wild type and mutant worms are healthy adults with similar appearance, except ire-1(v33), which is clearly smaller than the other strains ( Figure 2A ). In the presence of lowmoderate levels of the PFT Cry5B, wild-type worms are slightly intoxicated compared to those found on control no-toxin plates, as evidenced by their smaller sizes and paler appearances (Figure 2A ). To the same extent seen with wild-type worms, atf-6(ok551) and pek-1(ok275) mutant animals are also slightly intoxicated on lowmoderate levels of the PFT Cry5B, indicating lack of either of these genes does not result in overt hypersensitivity or hyperresistance to Cry5B (Figure 2A) . However under the same conditions, the ire-1(v33) and xbp-1(zc12) mutant worms are more severely intoxicated than wild-type worms as they are relatively smaller and considerably paler compared to their corresponding no toxin controls. The hypersensitivity to Cry5B resulting from lack of ire-1 and xbp-1 was also seen using RNA interference (RNAi; data not shown), confirming the phenotype is caused by loss of function in these genes. We call this hypersensitivity phenotype ''Hpo'' for hypersensitive to pore-forming toxin.