Homozygous females produce embryos that arrest prior to cellularisation. Embryos derived from cnn^mfs1/Df(2R)cnn females have severe defects in nuclear division and distribution. 8% of embryos arrest development before cortical migration. These embryos have large aggregates of chromosomes in the interior, but are devoid of nuclei at the cortex. The rest of the embryos accomplish cortical migration but never achieve cellularisation.

Cytokinesis and karyokinesis during meiotic divisions are disrupted in cnn^mfs1/Df(2R)cnn males; various numbers of nuclei are associated with nebenkern (suggesting failure of cytokinesis), and some cysts have nuclei of unequal sizes (suggesting failure of karyokinesis). The percentage of aberrant spermatids varies from testis to testis (20-50%), and the cytokinetic defects are more severe than karyokinetic defects. The microtubule network is morphologically normal in primary spermatocytes, although at the transition to meiotic division I, the prominent asters seen in wild-type spermatocytes do not form in cnn^mfs1/Df(2R)cnn spermatocytes. Some spermatocytes have regions of high microtubule density, and in many cases only one focus of higher microtubule density can be distinguished. Spindle defects are seen, including spindles with one focused pole and one diffuse pole, and cysts with multipolar spindles and disorganised microtubules. The midzone microtubules do not form. Multiple axonemes with various numbers of mitochondrial derivatives occupy one membrane system in stage 17 spermatids, and the axonemes are structurally abnormal; 40% of axonemes have no central pair of microtubules and 20% have only one central microtubule.