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Seizure Suppression by shakB², a Gap Junction Mutation in Drosophila

¹Department of Environmental Science, Policy and Management, Division of Insect Biology and ²Department of Molecular and Cell Biology, Division of Neurobiology, University of California, Berkeley, California

Submitted 7 October 2005; accepted in final form 23 September 2005

Gap junction proteins mediate electrical synaptic transmission. In Drosophila, flies carrying null mutations in the shakB locus, such as shakB², have behavioral and electrophysiological defects in the giant fiber (GF) system neurocircuit consistent with a loss of transmission at electrical synapses. The shakB² mutation also affects seizure susceptibility. Mutant flies are especially seizure-resistant and have a high threshold to evoked seizures. In addition, in some double mutant combinations with "epilepsy" mutations, shakB² appears to act as a seizure-suppressor mutation: shakB² restores seizure susceptibility to the wild-type range in the double mutant. In double mutant combinations, shakB² 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 shakB². Seizures caused by bang-sensitive (bas²) and bang-senseless (bss¹, bss² alleles) mutations are not suppressed by shakB². 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.

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