Fig. 5. Genetic interactions among unc-5, unc-6, unc-40, unc-51 and unc-14. (A-C) To analyze the axon-guidance defects of the mutants, we counted the number of DD/VD axons that could reach the dorsal nerve cord in L4 larvae or young adults. At least 20 worms were examined and the results were averaged for each strain. unc-5(e53)/+ and unc-40(n324)/+ represent the heterogygote of each of mutants. Error bars show the standard error. ^*1, P<0.01; NS, not significant (Bonferroni correction). (A) Genetic interactions among unc-5, unc-51 and unc-14. The low dose of unc-5 strongly enhanced the defects of both unc-51 and unc-14 (^*1). ^*2, unc-14(e57) did not enhance the phenotype of unc-51(e369), indicating that these genes were in the same genetic pathway for axon guidance. (B) Genetic interactions among unc-6, unc-51 and unc-14. ^*3, strong enhancement of mutant phenotypes by unc-6(ju152). (C) Genetic interactions between unc-40 and unc-51. The low dose of unc-40 did not enhance the defects of unc-51. In these analyses, we used hT2 (I, III) balancer for a making the heterozygote strain of unc-40(n324). As the balancer strain includes qIs48 that expresses GFP at the pharynx, we could not analyze one axon that passed near the pharynx. We excluded the axon from our counting.