ctp^e73 pupae fail to destroy their salivary glands by 12 hours after head eversion.

In ctp^e73 flies, the axons of the femoral chordotonal organ show abnormal terminal branching. The first defects occur at about 20h APF, somewhat earlier than for Gl¹ mutants, but otherwise are very similar to those caused by Gl¹. Haltere axons and hair plate axons are unaffected.

Thinner and shorter macrochaetae on notum, head and legs and moderate reduction in the number of notal microchaetae. ctp¹/ctp^e73 transheterozygotes are semi-viable and exhibit the same macro- and microchaetae embryonic phenotype as the homozygotes. Late pupae exhibit CNS defects. Tactile neurons project abnormally within the pupal CNS so the anterior bundles of axons in the pro- and mesothoracic neuromeres are enlarged, the posterior projections are smaller than normal. Club neurons from the femoral chordotonal organ show anteriorly shifted trajectories in the prothoracic neuromere but the axons terminate in the normal target region. Axons of the anterior chordotonal organ of Power are often deflected to an anterior tract as they cross the T1 neuromere but the axons terminate in the normal target region. Claw like neurons of the femoral chordotonal organ exhibit an altered projection pattern due to alteration, addition or deletion of branches and defasciculation. Low frequency of defects can be seen in the embryonic CNS; defects in the longitudinal connectives and commissural tracts.