Khc¹⁷/Khc²⁷ larvae show paralytic tail flipping on normal or rich food that is remarkably suppressed on poor food. Khc¹⁷/Khc²⁷ animals show pupal lethality on poor, normal and rich food.

Khc¹⁷/Khc²⁷ larvae show reduced flux of both neurosecretory dense core vesicles and mitochondria along the axons compared to wild type.

Results in larval posterior paralysis in combination with a null Khc allele.

Both anterograde and retrograde flux of axonal mitochondria is inhibited in Khc¹⁷/Khc²⁷ larvae.

28% of eggs from females containing homozygous germline clones show defects in dorsal appendage morphology; 24% have fused dorsal appendages and 4% have reduced dorsal appendages.

The velocity of ooplasmic streaming in stage 10B oocytes is reduced in mutant females compared to wild type.

In Khc¹⁷/Khc²⁷ larval motor axons, the anterograde and retrograde flux of mitochondria is reduced by 70-90%. The number of mitochondria in these mutant nerves is reduced by 50.5% in segments A2-A3.

Approximately 4% of Khc¹⁷ mutants are embryonic lethal, with 22% lethal in the larval/pupal stages and approximately 74% of Khc¹⁷ embryos surviving till adulthood. Some Khc¹⁷ oocytes exhibit minor slow streaming currents, but most endosomes show only short-range saltation. The few streaming movements do not contribute substantially to the mean velocity of randomly selected endosomes, which is approximately 2.4-fold less than wild-type. At stage 10B-11, Khc¹⁷ oocytes exhibit saltation and short, individual endosome displacement along with concerted fast-streaming currents, in 27% of cases. In approximately 10-15% of cases, weak streaming occurs throughout the oocyte. In another 10-15%, streaming is restricted to smaller regions. Randomly selected endosomes have a mean velocity approximately 7-fold less than in wild-type.

Hemizygotes sometimes survive to adulthood.