Hemizygous ovaries have relatively normal egg chambers, although the oocyte is often in an abnormal position.

Females have small ovaries, development begins to arrest at stage 4 or 5 of oogenesis and leads to the accumulation of a chain of spherical egg chambers during early oogenesis. Egg chambers remain small during subsequent stages and many degenerate after mid-oogenesis. Actin cytoskeleton is disrupted in ovaries. Follicle cells function normally. Posterior migration of the follicle cells occurs normally but they secrete reduced dorsal appendages and an 'open-ended' chorion.

Females exhibit reduced quantities of yolk in the oocytes due to defects in the uptake mechanism of vitellogenin: complete failure of endocytotic vitellogenin uptake from the haemolymph. Wild type ovaries transplanted into mutant females develop normally but mutant ovaries transplanted into wild type females do not develop normally. Results demonstrate the ability to take up vitellogenin from the haemolymph is attributable to developmental defects within the ovary.

Many egg chambers, some have abnormal numbers of nurse cells, many degenerate, some form eggs with abnormal chorions.