Song, Juan and Mark A. Tanouye. Seizure suppression by shakB 2 , a gap junction mutation in Drosophila. . Gap junction proteins mediate electrical synaptic transmission. In Drosophila, flies carrying null mutations in the shakB locus, such as shakB 2 , have behavioral and electrophysiological defects in the giant fiber (GF) system neurocircuit consistent with a loss of transmission at electrical synapses. The shakB 2 mutation also affects seizure susceptibility. Mutant flies are especially

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... re-resistant and have a high threshold to evoked seizures. In addition, in some double mutant combinations with "epilepsy" mutations, shakB 2 appears to act as a seizure-suppressor mutation: shakB 2 restores seizure susceptibility to the wild-type range in the double mutant. In double mutant combinations, shakB 2 completely suppresses seizures caused by slamdance (sda), knockdown (kdn), and jitterbug (jbug) mutations. Seizures caused by easily shocked (eas) and technical knockout (tko) mutations are partially suppressed by shakB 2 . Seizures caused by bang-sensitive (bas 2 ) and bang-senseless (bss 1 , bss 2 alleles) mutations are not suppressed by shakB 2 . These results show the use of Drosophila as a model system for studying the kinds of genetic interactions responsible for seizure susceptibility, bringing us closer to unraveling the complexity of seizure disorders in humans.