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, Joyce Yu

Research output: Contribution to journalArticlepeer-review

39 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)2988-2993
Number of pages6
JournalJournal of Neuroscience
Volume20
Issue number8
DOIs
StatePublished - Apr 15 2000

Keywords

  • Behavior
  • Calcium-activated potassium channel
  • Drosophila
  • Flight
  • Potassium channel
  • Regulation of transcription
  • Tissue-specific transcription

ASJC Scopus subject areas

  • Neuroscience(all)

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