enhancer of seizure: A New Genetic Locus in Drosophila melanogaster Defined by Interactions With Temperature-Sensitive Paralytic Mutations

Durgadas P. Kasbekar ¹, James C. Nelson ², and Linda M. Hall ¹

¹ Department of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461
² Department of Biology, Yale University, New Haven, Connecticut 06511

Mutations in the enhancer of seizure (e( sei)) locus have been isolated on the basis of their ability to cause temperature-induced paralysis of alleles at the seizure (sei ) locus at temperatures at which these mutations ordinarily do not paralyze. This enhancer is specific to the seizure locus and is without effect on other temperature-sensitive paralytic mutants including para, nap, tip-E and shi. This suggests that the enhancer responds specifically to the mechanism of paralysis mediated by the seizure mutations. The e(sei) is a recessive mutation which maps to 39.0 on the left arm of chromosome 3. Deficiency mapping has placed it at 69A4-B5 on the salivary gland polytene chromosome map. When a new enhancer allele was isolated following P-M hybrid dysgenesis, there was a concomitant P-element insertion at 69B. In the absence of seizure mutations, the enhancer mutation causes non-temperature dependent hyperactivity when agitated and interferes with the climbing response. Electrophysiological studies examined the effects of increasing temperature on electrical activity in the adult giant fiber/flight muscle system. Neuronal hyperactivity was seen in both e(sei) and sei single mutant homozygotes, but not in wild type. The hyperactivity was more severe in the sei; e(sei) double mutants. The correlation between the physiological effects and the mutant behavior suggests that both sei and e (sei) cause membrane excitability defects. Since previous work has shown that seizure mutants affect [³H]saxitoxin binding to the voltage-sensitive sodium channel, e(sei) may code for a gene product which interacts with this channel.

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