Complementation of Physiological and Behavioral Defects by a Slowpoke Ca super(2+)-Activated K super(+) Channel Transgene

• Published in: Journal of neurochemistry Vol. 75; no. 3; pp. 1310 - 1319
• Main Authors: Brenner, R, Yu, J Y, Srinivasan, K, Brewer, L, Larimer, J L, Wilbur, J L, Atkinson, N S
• Format: Journal Article
• Language: English
• Published: 01.09.2000
• Subjects: Drosophila; slowpoke gene
• ISSN: 0022-3042

The Drosophila slowpoke gene encodes a large conductance calcium-activated potassium channel used in neurons, muscle, and some epithelial cells. Tissue-specific transcriptional promoters and alternative mRNA splicing generate a large array of transcripts. These distinct transcripts are thought to tailor the properties of the channel to the requirements of the cell. Presumably, a single splice variant cannot satisfy the specific needs of all cell types. To test this, we examined whether a single slowpoke splice variant was capable of complementing all slowpoke behavioral phenotypes. Null mutations in slowpoke cause animals to be semiflightless and to manifest an inducible "sticky- feet" phenotype. The well-characterized slowpoke transcriptional control region was used to direct the expression of a single slowpoke splice variant (cDNA H13) in transgenic flies. The endogenous gene in these flies had been inactivated by the slo super(4) mutation. Action-potential recordings and voltage-clamp recordings demonstrated the production of functional channels from the transgene. The transgene completely complemented the flight defect, but not the sticky-feet phenotype. We conclude that distinct slowpoke channel isoforms, produced by alternative splicing, are not interchangeable and are required for proper function of different cell types.