The actin cytoskeletons of mutant photoreceptor cells appear largely normal, with well-formed rhabdomere terminal webs.

In mosaic eyes containing large homozygous didum^Q1052st clones, mutant photoreceptors have small rhabdomeres.

Ectopic rhabdomeres on the photoreceptors are common in mosaic eyes containing homozygous didum^Q1052st clones. Ectopic rhabdomeres are occur, but are less common, in didum^Q1052st adult escapers.

Abnormal vesicles crowd the mutant photoreceptor cytoplasm in eyes containing homozygous clones. The vesicles appear empty, with irregular profiles typically 200-400nm across (this is substantially lager than normal secretory vesicles).

didum^Q1052st larvae experience delayed development; the length of the second instar is expanded by ~2 days and didum^Q1052st second instar larvae appear smaller than didum^Q1052st/+ larvae by day 3. Less than 10% of didum^Q1052st larvae pupate, and pupation is late. Very few didum^Q1052st mutants manage to eclose. Escaper didum^Q1052st adults have normal rhabdomere structure and display normal behaviour in response to light. Female fertility is not affected in didum^Q1052st mutants. Both didum^Q1052st adult female escapers and females carrying didum^Q1052st germline clones are able to produce viable offspring. didum^Q1052st male adult escapers are sterile. didum^Q1052st mutants mate with females but no offspring are produced as a result. Investigation into spermatogenesis shows that early stages, up to cyst elongation, appear unaffected. However, the process of sperm individualization appears to be defective. The investment cones, actin-based structures that normally assemble around spermatid nuclei at the start of individualization, are scattered and poorly associated with nuclei in the mutants. Investment cones that are observed with nuclei frequently fail to extend past those nuclei. No complete individualization complexes are ever formed, leading to an absence of motile sperm within the seminal vesicles of didum^Q1052st males.