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 neurons and muscles and cause behavioral defects. The animals fly very poorly compared with wild-type strains and, after exposure to a bright but cool light or a heat pulse, exhibit a "sticky-feet" phenotype. Expression of slowpoke arises from five transcriptional promoters that express the gene in neural, muscle, and epithelial tissues. A chromosomal deletion (ash2(18)) has been identified that removes the neuronal promoters but not the muscle-tracheal cell promoter. This deletion complements the flight defect of slowpoke null mutants but not the sticky-feet phenotype. Electrophysiological assays confirm that the ash2(18) chromosome restores normal electrical properties to the flight muscle. This suggests that the flight defect arises from a lack of slowpoke expression in muscle, whereas the sticky-feet phenotype arises from a lack of expression in nervous tissue.
Atkinson
N S
NS
Section of Neurobiology, School of Biological Sciences, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas 78712-1064, USA. nigela@mail.utexas.edu
Brenner
R
R
Chang
W m
Wm
Wilbur
J
J
Larimer
J L
JL
Yu
J
J
D000200:Action Potentials / Q000235:genetics*; D000818:Animals; D004330:Drosophila; D005426:Flight, Animal / Q000502:physiology*; D017353:Gene Deletion; D010641:Phenotype; D015221:Potassium Channels / Q000235:genetics*; D011401:Promoter Regions, Genetic / Q000235:genetics*
D015221:Potassium Channels