Complementation of physiological and behavioral defects by a slowpoke Ca2+-activated K+ channel transgene

Robert Brenner, Joyce Y. Yu, Karpagam Srinivasan, Lawrence Brewer, James L. Larimer, Jennette L. Wilbur, Nigel S. Atkinson

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


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 slo4 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.

Original languageEnglish (US)
Pages (from-to)1310-1319
Number of pages10
JournalJournal of neurochemistry
Issue number3
StatePublished - 2000
Externally publishedYes


  • Behavior
  • Drosophila
  • Potassium channel
  • Slowpoke
  • Voltage clamp
  • mRNA splicing

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


Dive into the research topics of 'Complementation of physiological and behavioral defects by a slowpoke Ca2+-activated K+ channel transgene'. Together they form a unique fingerprint.

Cite this