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The Journal of Neuroscience, April 15, 2000, 20(8):2988-2993

Molecular Separation of Two Behavioral Phenotypes by a Mutation Affecting the Promoters of a Ca-Activated K Channel

Nigel S. Atkinson, Robert Brenner, Whei-meih Chang, Jennette Wilbur, James L. Larimer, and Joyce Yu

Section of Neurobiology, School of Biological Sciences and the Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas 78712-1064

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 (ash2¹⁸) 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 ash2¹⁸ 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.

Key words: Drosophila; calcium-activated potassium channel; potassium channel; behavior; flight; tissue-specific transcription; regulation of transcription

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Copyright © 2000 Society for Neuroscience  0270-6474/00/2082988-06$05.00/0

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