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Volume 17, Number 3, Issue of February 1, 1997 pp. 882-890
Copyright ©1997 Society for Neuroscience

The seizure Locus Encodes the Drosophila Homolog of the HERG Potassium Channel

Received July 9, 1996; revised Nov. 15, 1996; accepted Nov. 18, 1996.

XinJing Wang, Elaine R. Reynolds, Péter Déak, and Linda M. Hall

¹ Department of Biochemical Pharmacology, State University of New York at Buffalo, Buffalo, New York 14260-1200

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.

Key words: cloned potassium channel; Drosophila melanogaster; gene mapping; seizure gene; hyperexcitability; temperature-induced paralysis; sodium channel regulation; transformation; transgenic animals; HERG; I_Kr; eag gene family; ion channel turn over

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