Mutants show male sterility, with highly elongated, immobile, blebbed sperm tails, disrupted individualisation complexes and scattered spermatid nuclei. Mutants construct more individualisation complexes than do nkg mutants. The ICs fail to progress along the spermatogenic cyst. Earlier stages of spermatogenesis also show defects, for example in nebenkern formation (nebenkerns are lacking in many onion-stage spermatids).