Figure 7.

Genetic interactions between null alleles of CSAS and DSiaT analyzed by behavioral assays. A, Interactions between null alleles of CSAS and DSiaT analyzed by TS-paralysis assays. While CSAS and DSiaT single mutants show a quantitatively similar TS-paralysis phenotype, the paralysis of CSAS-DSiaT double mutants is more severe than that of the single mutants. For the genotype combining a homozygous mutation in one gene with a heterozygous mutation of another gene, the phenotypes are not significantly different from each other and from the phenotypes of single homozygous mutants. At least 20 flies (males) were assayed for each genotype.DSiaT^L22/+ CSAS^Df/+, double heterozygote for CSAS and DSiaT combining one copy of null mutation for each gene; DSiaT^L22/s23, heteroallelic DSiaT mutant combining two null alleles; DSiaT^L22/L22, homozygous null mutant; CSAS^21/21, homozygous null mutant; DSiaT^L22/L22 CSAS^221/+, combination of DSiaT^L22 homozygote with CSAS²²¹ heterozygote; DSiaT^L22/+ CSAS^221/221, combination of DSiaT^L22 heterozygote with CSAS²²¹ homozygote; DSiaT^L22/L22 CSAS^221/221, double homozygous null mutant for DSiaT and CSAS. B, Interactions analyzed by locomotion assays. CSAS and DSiaT homozygous single mutants have prominent locomotion phenotypes that are qualitatively and quantitatively indistinguishable from each other. At the same time, CSAS-DSiaT double mutants have a significantly stronger phenotype than that of single mutants. The locomotion defect of CSAS mutants can be fully rescued by transgenic expression of the CSAS-FLAG construct (CSAS⁺ CSAS^Mi/Df). See above and Figure 5 for explanation of genotypes. A, B, Statistical analysis was performed using one-way ANOVA followed by post hoc multiple-comparison Wilcoxon each pair test. **p < 0.01, ***p < 0.001, statistically significant differences; o, no significant differences (p > 0.24). Error bars are SEM.