Oogenesis is profoundly disturbed in hts¹/hts¹⁰⁰⁸⁹ mutants.

hts¹/hts¹⁰⁰⁸⁹ mutant ovaries contain numerous aborted egg chambers that lack ring canals and a clearly differentiated oocyte and never enter vitellogenesis.

Young, 1-4 day old hts¹/hts¹⁰⁰⁸⁹ mutant females expressing two copies of hts^{Δ100.αTub84B} display a number of egg chambers that are able to complete oogenesis, with most of the resulting eggs (~60%) able to support embryogenesis to at least the larval stage. Ovaries from these females contain developing egg chambers of various stages, and also egg chambers that have arrested prior to vitellogenesis. All egg chambers in these flies contain ring canals, even those that have failed to mature. As these females get older, the aborted egg chambers accumulate in the ovaries, resulting in an overall failure of oogenesis.

hts¹/hts¹⁰⁰⁸⁹ mutant females expressing two copies of hts^{Δ100.αTub84B} only rarely (~5%) contain ectopic actin aggregates.

In contrast to wild type, many spermatocytes in hts¹/hts¹⁰⁰⁸⁹ mutants contain too many or too few centrosomes.

In contrast to wild type, 6% of meiotic spermatocytes in hts¹/hts¹⁰⁰⁸⁹ mutant testes show spindle abnormalities, including monopolar and multipolar spindles.

Complete loss of fusome in the adult ovary cells.

Homozygous females produce egg chambers with less than 15 nurse cells and these egg chambers usually degenerate before completing oogenesis. Most egg chambers lack an oocyte. Ring canals in cysts and egg chambers are reduced in number and have deformed outer rings. Phalloidin staining revealed that the abnormal ring canals were deficient in actin. Homozygotes show reduced viability and rough eyes.