Hvir\βt fails to support any microtubule assembly in βTub85D null mutants. When coexpressed with βTub85D, Hvir\βt poisoned all microtubule-mediated processes; spermatid nuclei are not shaped, spermatids are not aligned, spermatid elongation is defective, reflecting failure of axoneme assembly and mitochondrial derivative elongation.
Drives expression in the postmitotic male germ cells with correct developmental specificity. When Hvir\βt composes more than 6% of the total β-tubulin pool males are sterile.