RT Journal Article
SR Electronic
T1 The <em>seizure</em> Locus Encodes the <em>Drosophila</em>Homolog of the HERG Potassium Channel
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 882
OP 890
DO 10.1523/JNEUROSCI.17-03-00882.1997
VO 17
IS 3
A1 XinJing Wang
A1 Elaine R. Reynolds
A1 Péter Déak
A1 Linda M. Hall
YR 1997
UL http://www.jneurosci.org/content/17/3/882.abstract
AB Mutations in the seizure (sei) locus cause temperature-induced hyperactivity, followed by paralysis. Gene cloning studies have established that the seizuregene product is the Drosophila homolog ofHERG, 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 thesei 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 at1/2 of ∼1-1.5 d after gene induction is discontinued, providing the first estimate of ion channel stability in an intact, multicellular animal.