Centriolar association with the nucleus appears normal in primary spermatocytes in homozygous males. However, some disruption in the association between the nucleus and centrioles is seen starting at the round spermatid stage, and this defect becomes more pronounced and fully penetrant as the nuclei condense and elongate. In later elongation stages, the basal bodies are scattered along the nuclear bundles and the nuclei are frequently contorted.

Homozygous mutants show failures in sperm individualization. Axoneme structure appears grossly normal and arrays of axonemes each associated with a single major and minor mitochondrial derivative are seen (as occurs in wild type). However, both mitochondrial derivatives fail to condense fully (this defect is most severe for the minor mitochondrial derivative), plasma membrane investment largely fails to occur and copious amounts of cytoplasm remain in the mutant cysts. The individual actin cones are disrupted during individualization, with cones no longer forming organised individualization complexes and in bundles of contorted nuclei, actin cones are often missing altogether. The disorganised individualization complexes tend not to progress caudally and mutant testes lack cytoplasmic bulges and waste bags.

Despite the failures in sperm individualization, the elongated syncytial cysts attempt the final coiling process that normally precedes sperm movement into the seminal vesicles and thus the terminal region of mutant testes is filled with coiling cysts.

No mature sperm accumulates in the seminal vesicles of homozygous males sequestered for several says away from females (the seminal vesicles of wild-type males fill with mature sperm under these conditions).