Homozygous males show a completely penetrant sterility phenotype. The testes of homozygous males show defects in spermatogenesis, with the severity of the phenotype ranging from testes that lack properly elongated spermatids to testes that look almost normal but lack mature sperm.

Spermatocytes and onion stage spermatids look normal in homozygous testes. Early elongating spermatids show signs of of delayed elongation. Often, abundant white structures of unknown origin are seen in spermatid bundles. Mitochondrial derivatives of elongating and elongated spermatids sometimes have bulby protrusions that are reminiscent of unelongated or improperly elongated mitochondrial derivatives. Mature sperm are never seen. At the ultrastructural level, homozygous spermatid cysts are unorganised. The major and minor mitochondrial derivatives are often impossible to distinguish from one another in the mutant testes. Often, one axoneme is associated with two mitochondrial derivatives of similar size and both have accumulated the paracrystalline structure (this structure is normally typical for the major mitochondrial derivative). In some cases, one mitochondrial derivative is extremely enlarged and contains heterogeneous accumulations of the paracrystalline structure. The nuclei of mutant spermatids are needle-shaped in elongated spermatids (as in wild type), but they are scattered over large areas of the length of the testis or form fuzzy bundles (in wild-type they are located at the base of the testis in parallely packed bundles). Actin cones are not seen in the mutant testes, although in one testis the association of f-actin with nuclei has been seen, which might be indicative for the formation of an individualization complex.

Homozygous males are completely sterile, regardless of whether they are raised on normal, low iron or high iron food.