stl³ and stl³/stl⁴ mutant embryos display significantly faster dorsal migration of the v'ch1 sensory neuron during stages 15-17, to its target the lch5 chordotonal organ cluster, as compared to wild type, and no over-migration past its target.

Ovaries of 10 day old stl³/stl⁴ females show severe degeneration.

Homozygous and stl^8-1204/stl³ ovarioles in adult females lack the interfollicular stalks that normally separate adjacent wild-type follicles. This phenotype results from failed follicle individualisation, rather than from persistent germline cell division, because mutant ovarioles contain germ cells at varying stages of maturation and groups of 16 interconnected germ cells that would correspond to a single germline cyst in wild-type are still recognisable. Degeneration is seen in the mutant ovarioles, which increases with age, and both germline and somatic cells appear to degenerate. Homozygous somatic clones in the ovariole can be recovered. Mutant clones in somatic epithelial cells are variably associated with follicular defects. Severe stl-like follicle formation defects are most often associated with very large somatic homozygous clones in the ovary, but not every large mutant clone in the ovary results in severe defects. The mosaic analysis also suggests that weak follicular defects are often due to an effect of nonovarian mutant clones. Wild-type ovaries transplanted into the abdomens of homozygous male hosts show severe morphological defects (wild-type ovaries transplanted into the abdomens of wild-type male hosts are morphologically normal).

Germline cysts accumulate in an enlarged germarium in stl⁴/stl³ females.

Abnormal numbers of nurse cells and tumorous egg chambers.