Figure 1.

Characterization of the Khc²⁰ and Khc²⁷ alleles. (A) An allele that causes a partial loss of function, Khc⁶, was used to compare the severities of Khc²⁰, Khc²⁷, and a deletion that removes the Khc locus (Df(2R)Jp6). Each point represents the percentage of animals that survived to the beginning of the indicated stage of development. The numbers of larvae tested for each combination were Khc⁶/Khc²⁰, n = 138; Khc⁶/Khc²⁷, n = 179; and Khc⁶/Df(2R)Jp6, n = 114. The lethal effects of Khc²⁰, Khc²⁷, and the deletion were indistinguishable. (B) Western blot of cytosol from male flies with the following genotypes: (lane 1) Khc²⁰/Khc²⁰; P{w⁺, c-myc-Khc⁺}/+; (lane 2) Khc²⁷/Khc²⁷; P{w⁺, c-myc-Khc⁺}/+; (lane 3) Df(2R)JP6/Khc⁺; P{w⁺, c-myc-Khc⁺}/+; (lane 4) Khc⁺/Khc⁺. Equal amounts of protein were loaded in each lane. The blot was probed with an antibody that binds to the amino-terminal motor domain of Drosophila KHC (Brendza et al., 1999). The P{w⁺, c-myc-Khc⁺} transgene produced a Myc-KHC fusion protein that rescued the Khc mutants. Its slower electrophoretic mobility allowed detection of KHC produced by endogenous genes (lane 3). No endogenous KHC was detected in flies that were homozygous for Khc²⁰ or Khc²⁷ (lanes 1 and 2).