Genetic interaction of SLO-1/BK and UNC-2/CaV2 channels. (A) SLO-1/BK functionally interacts with UNC-2/CaV2 channels for locomotory behavior. A gain-of-function unc-2(zf35) mutation suppresses the sluggish movement of slo-1(gf) mutants, whereas dgk-1 mutation, which causes a hyperactive phenotype, does not. The data are presented as the mean ± SEM and analyzed by one-way ANOVA with Bonferroni’s post Hoc test (**p < 0.01, n.s., not significant). (B and C) A loss-of-function unc-2 mutation increases the SLO-1 punctal density in the presynaptic region. The number of SLO-1 puncta in a given length of the axonal terminal (i.e., decreased punctal distance) is higher in unc-2 mutants than wild-type or unc-13 animals. The quantification of SLO-1 puncta number was performed in cimIs10 animals whose genetic background is wild-type, unc-2 or unc-13 animals. The data are presented as the mean ± SEM and analyzed by two-tailed Student t-test (wild-type, n = 14; unc-2, n = 11; unc-13, n = 12 ***p < 0.001, n.s., not significant). Scale bar, 5 μm.