Mutant testes have ring canals (RCs) of variable sizes. The RCs present in spermatogonia and primary spermatocytes are usually normal. These apparently normal RCs persist throughout meiosis and are also found in spermatids. However, 12% of spermatids also show larger, often severely misshaped RC-like structures. These spermatids usually have a large nebenkern and 4 normally-sized nuclei.

The central spindle is severely defective in the first meiotic division in homozygous males, and the actin ring is usually missing.

Transmission rate of Dp(1;f)J21A through females to progeny is 28%, Klp3A mutation strongly decreases transmission. Mutation also decreases transmission of Dp(1;f)1B, Dp(1;f)25A and Dp(1;f)10B.

Over 90% eggs laid do not hatch into larvae, of these over 80% contain sperm tails so the primary block in development must occur after fertilisation. The large majority undergo very few if any nuclear divisions. In the terminal state the presumptive female pronucleus remains associated with the other 3 products of female meiosis in a single polar body. The male pronucleus remains separated a considerable distance from this polar body. Although the gonomeric spindle cannot be formed in these conditions a bipolar spindle is established around the haploid paternal genome. A significant minority of embryos develop past this point and display mitotic defects (disorganised spindles, unequal spacing of nuclei and free centrosomes). At gastrulation these embryos display a range of apparently nonspecific defects accompanied by cellular degradation. Examination of the cuticles reveals variable defects in cuticle formation and incomplete segmentation. Some rare embryos escape and hatch into larvae, almost all of these develop into normal adults. Adult male and female escapers are recovered in equal proportions. None of these adults are aneuploid for the X or 4th chromosome suggesting chromosome segregation during meiosis in eggs is generally regular.