Neurogenetic analysis of Drosophila mutations affecting sodium channels: synergistic effects on viability and nerve conduction in double mutants involving tip-E.
In previous work it was shown that parats (paralyzed, temperature-sensitive, 1-53.9) and napts (no action potential, temperature-sensitive, 2-56.2), two temperature-sensitive paralytic mutations that block nerve conduction at restrictive temperatures, interact synergistically in double mutants causing unconditional lethality. This interaction is now shown to include tip-E (temperature-induced paralysis, 3-13.5), another temperature-sensitive paralytic mutation. There is an allele-dependent interaction between tip-E and various para alleles resulting in the unconditional lethality of the most extreme double mutant combinations. The pattern of this allele-dependency is strikingly different from that previously reported for napts and para in that the para alleles that interact strongest with napts interact weakest with tip-E and vice-versa. Double mutants of tip-E with napts also display greatly reduced viability. Surviving double mutants of tip-E with either parats1 or napts are weak and exhibit enhanced temperature sensitivity for both paralysis and nerve conduction failure. In addition, in a tip-E background, mutant para alleles enhance temperature-sensitive paralysis even when heterozygous with para+. The results of these studies suggest that tip-E shares related function with para and nap. It is proposed that tip-E, like para and nap exerts an effect at some level on the structure, function, or stability of sodium channels.