Figure 4. PLCβ and PLCγ function, through the production of an IP₃ signal, in the aversive response to nose touch, but not to benzaldehyde.

(A) Reversal response of PLC deficient animals to nose touch. All showed a wild type response (>90% reversing >1 worm length) to anterior body touch (data not shown). (B) Reversal response of itr-1(sy290) gain-of-function animals to nose touch, following depletion of plc-3 or egl-8 by RNAi. CAT, E. coli chloramphenicol acetyltransferase. All showed a wild type response (>90% reversing >1 worm length) to anterior body touch (data not shown). (C) Reversal response of PLC deficient animals to benzaldehyde. All showed a wild type response (<5% reversing >1 worm length) to buffer alone (data not shown). Both plc-3 and egl-8 loss-of-function mutants exhibit defective responses to nose touch (P<0.001) compared to wt animals. RNAi of plc-3 or egl-8 similarly disrupted the response (P<0.001) compared to the CAT(RNAi) control animals. However, RNAi of plc-3 or egl-8 in an itr-1(sy290) background failed to disrupt the response to such an extent (plc-3, P<0.001; egl-8, P<0.05, when compared to RNAi of the same genes in wt animals). All P values are from Chi-squared tests.