The seizure locus encodes the Drosophila homolog of the HERG potassium channel

Xinjing Wang, Elaine R. Reynolds, Péter Déak, Linda M. Hall

Research output: Contribution to journalArticle

57 Citations (Scopus)

Abstract

Mutations in the seizure (sei) locus cause temperature-induced hyperactivity, followed by paralysis. Gene cloning studies have established that the seizure gene product is the Drosophila homolog of HERG, a member of the eag family of K+ channels implicated in one form of hereditary long QT syndrome in humans. A series of five null alleles with premature stop codons are all recessive, but viable. A missense mutation in the sei gene, which changes the charge at a conserved glutamate residue near the outer mouth of the pore, has a semidominant phenotype, suggesting that the mutant seizure protein acts as a poison in a multimeric complex. Transformation rescue of a null allele with a cDNA under the control of an inducible promoter demonstrates that induced expression of seizure potassium channels in adults rescues the paralytic phenotype. This rescue decays with a t(1/2) of 1-1.5 d after gene induction is discontinued, providing the first estimate of ion channel stability in an intact, multicellular animal.

Original languageEnglish
Pages (from-to)882-890
Number of pages9
JournalJournal of Neuroscience
Volume17
Issue number3
DOIs
Publication statusPublished - Jan 1 1997

Keywords

  • Drosophila melanogaster
  • HERG
  • I(Kr)
  • cloned potassium channel
  • eag gene family
  • gene mapping
  • hyperexcitability
  • ion channel turn over
  • seizure gene
  • sodium channel regulation
  • temperature-induced paralysis
  • transformation
  • transgenic animals

ASJC Scopus subject areas

  • Neuroscience(all)

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