Mutations in and RNAi-mediated knockdown of Clic reduce ethanol sensitivity in ethanol sedation assaysST50s were greater in homozygous ClicG0472 (A) and ClicEY04209 (B) transposon mutants (closed bars) than in w1118 controls (open bars) (*individual t tests, p≤0.027, n=10 per genotype) in ethanol sedation assays with vapor from 50% ethanol. Control and Clic mutant flies were reared at 20°C to circumvent homozygous lethality of the Clic alleles at 25°C. Ubiquitous (via da-Gal4, panel C, filled bar) or nervous system (via elav-Gal4, panel D, filled bar) expression of RNAi targeting Clic (v105975) lowered ethanol sensitivity compared to Gal4/+ and v105975/+ controls (open bars) (individual one-way ANOVAs, p<0.0001; *Bonferroni, p<0.05 compared to controls; n=8–10 per group). Internal ethanol concentrations were not consistently different in ubiquitous (E) and nervous system (F) Clic knockdown flies compared to Gal4 and v105975 controls (individual one-way ANOVAs; panel E, p=0.0288; panel F, p=0.0003; n=5; *Bonferroni’s multiple comparisons test, p<0.05 compared to Gal4 controls). Controls are (A) w1118 in a Canton-S background, (B) 2202U, (C) WTB, and (D) the progeny from NPFR1-Gal4 or NPFR1-RNAi crossed to our standard w1118 strain.
