To independently confirm these results, we used a developmental assay to assess the relative sensitivity of the four ER stress response mutants to Cry5B. This experiment was performed by placing newly hatched L1 stage worms on plates containing different percentages of Cry5B expressing E. coli and then counting the worms that developed to either the L4 stage or adulthood ( Figure 2C ). In the absence of Cry5B, nearly all worms developed to the L4 stage or adulthood for all strains with the exception of ire-1(v33). This result confirms developmental defects previously seen with this mutant [11] , and it was therefore excluded from subsequent analyses. Wild type N2 and pek-1(ok275) were both similarly inhibited in their development by increasing percentages of Cry5B. Compared to N2 and pek-1(ok275) animals, though, both atf-6(ok551) and xbp-1(zc12) were Hpo, i.e., each is more developmentally inhibited by Cry5B than wild-type animals ( Figure 2C ). Because the ire-1-xbp-1 pathway has a more discernible effect on protection against Cry5B than atf-6, further experiments were focused on this arm of the ER stress response.