Figure 5.

sdn-1 mutant neurodevelopmental and behavioral defects are dependent on TRPC channels in C. elegans. (A) In wt animals, PVQ neurons extend anteriorly-directed axons from the tail. The axons navigate the left and right ventral nerve cord fascicles where axons are separated by the hypodermal ridge. In sdn-1(zh20) mutant animals, PVQ axons are misguided, with crossover to the contralateral side of the ventral nerve cord (red arrowhead). In wt animals, HSN cell bodies migrate to a position just posterior to the vulva and extend axons in a highly stereotypical manner. Their axons extend ventrally, and then around the vulva before entering the ventral nerve cord where each axon is separated by the hypodermal ridge. In sdn-1(zh20) mutant animals, HSN cell bodies do not migrate to their correct position and their axons are misguided. Cell bodies are shown with white arrowheads and misguided axons by red arrowheads. Vulval position is marked with red asterisks. Ventral view, anterior to the left in all cases. Bar, 20 µm. (B and C) Scoring of PVQ and HSN developmental defects, respectively. n > 50 in each case. (D and E) Calcium imaging by FRET microscopy of ventral ganglia from live immobilized animals expressing the sensor cameleon YC3.60. n = 48–123 per strain. (F) Scoring of exploratory behavior; n > 15 for each strain. Data are the means ± SEM. Statistical significance was assessed by ANOVA followed by Newman-Keuls multiple comparison test. **, P < 0.01 versus sdn-1(zh20) mutant. Data in E were analyzed by ANOVA (P = 0.001) followed by pairwise t tests with Holm correction of p-values (wt vs. sdc null, P < 0.01; sdc null vs. sdc+TRP1/2 null, P < 0.005).