Journal of Neuroscience, Vol 7, 1307-1317, Copyright © 1987 by Society for Neuroscience
Gene dosage and complementation analysis of the Shaker locus in Drosophila
LC Timpe and LY Jan
Mutations of the Shaker (Sh) locus alter or eliminate a transient,
voltage-sensitive potassium current, the "A" current, in flight muscle of
Drosophila. We show that the amplitude of the A current is reduced when the
dosage of Sh+ is lower than normal, but that A current amplitude does not
increase as extra copies of Sh+ are added. We have also examined 14 Shaker
mutants by voltage clamp and by intracellular recording at the larval
neuromuscular junction. In 10 of these mutants there is no detectable fast
component of the transient outward current. In each of these 10, however, a
small, slowly inactivating, outward current is present. The 10 mutations
null for the fast component of the transient, outward current are all
partially dominant, giving 50-80% of the normal A current in Shnull/Sh+
heterozygotes. Because as little as 5% of the normal A current can be
detected, complementation tests are feasible. The 10 null mutations are
members of a single complementation group. The remaining 4 mutations have
reduced A currents in pupal flight muscle. In all cases, crosses between
these leaky mutants and null mutants give progeny with less A current than
found in the leaky parental lines, as would be expected if the leaky and
null mutations are in the same complementation group. For 1 of the
mutations, ShrKO120, the mutant phenotype is much more severe in nerve than
in muscle. That part of the Shaker locus required for the production of the
A channel lies between the B55 and the V7 translocation breakpoints, in
region 16F of the X chromosome.
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