PT  - JOURNAL ARTICLE
AU  - XinJing Wang
AU  - Elaine R. Reynolds
AU  - Péter Déak
AU  - Linda M. Hall
TI  - The <em>seizure</em> Locus Encodes the <em>Drosophila</em>Homolog of the HERG Potassium Channel
AID  - 10.1523/JNEUROSCI.17-03-00882.1997
DP  - 1997 Feb 01
TA  - The Journal of Neuroscience
PG  - 882--890
VI  - 17
IP  - 3
4099  - http://www.jneurosci.org/content/17/3/882.short
4100  - http://www.jneurosci.org/content/17/3/882.full
SO  - J. Neurosci.1997 Feb 01; 17
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.