Mutations in theseizure(sei) locus cause temperature-induced hyperactivity, followed by paralysis. Gene cloning studies have established that theseizuregene product is theDrosophilahomolog ofHERG, a member of theeagfamily 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 theseigene, 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 at1/2of ∼1-1.5 d after gene induction is discontinued, providing the first estimate of ion channel stability in an intact, multicellular animal.