Ns. Atkinson et al., Molecular separation of two behavioral phenotypes by a mutation affecting the promoters of a Ca-activated K channel, J NEUROSC, 20(8), 2000, pp. 2988-2993
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.