f01491 mutant flies would rescue the ethanol sedation phenotype of the mutant. The f01491 mutant flies were crossed to flies carrying elav-GAL4c155 to drive neuronal expression of dAlk from the P-element insertion in the f01491 mutant, which contains UAS sites in the orientation appropriate for GAL4-dependent transcription. The transcript expressed from the f01491 insertion contains the entire protein-coding region of dAlk, since the P-element is located 5′ of the ORF (Figure 2A). f01491 flies carrying the elav-GAL4 transgene exhibited normal ethanol sensitivity implying a complete rescue of the behavioral phenotype (Figure 2E, F), and indicating that dAlk expression in neurons is sufficient for normal ethanol sedation sensitivity. These results suggest that the normal function of dAlk is to promote enhanced sensitivity to ethanol. The behavioral response of dAlk mutants to ethanol is consistent with the negative regulation of dAlk by dLMO, since we have found that the function of dLMO is to promote resistance to the sedating effect of ethanol [20].
