Molecular separation of two behavioral phenotypes by a mutation affecting the promoters of a Ca-activated K channel

The Drosophila slowpoke gene encodes a BK-type calcium-activated potassium channel. Null mutations in slowpoke perturb the signaling properties of neu rons and muscles and cause behavioral defects. The animals fly very poorly compared with wild-type strains and, after exposure to a bright but cool li ght or a heat pulse, exhibit a "sticky-feet" phenotype. Expression of slowp oke arises from five transcriptional promoters that express the gene in neu ral, muscle, and epithelial tissues. A chromosomal deletion (ash2(18)) has been identified that removes the neuronal promoters but not the muscle-trac heal cell promoter. This deletion complements the flight defect of slowpoke null mutants but not the sticky-feet phenotype. Electrophysiological assay s confirm that the ash2(18) chromosome restores normal electrical propertie s to the flight muscle. This suggests that the flight defect arises from a lack of slowpoke expression in muscle, whereas the sticky-feet phenotype ar ises from a lack of expression in nervous tissue.