Homozygous clones generate cuticle patterning defects in the prescutum.
Homozygous clones induced in the third larval instar adopt a round and compact morphology and tend to segregate from the surrounding bowl[+] cells.
Somatic mutant clones induced in the antennal disc during L1 result in ectopic antennae formation, containing both proximal and distal antennal segments.
Mutant somatic clones in the ventral-posterior rim of the antennal disc lobe in L1 result in ventral eyelet formation and differentiation of mutant cells into photoreceptors in the adult eye.
Most homozygous clones generated at the early first larval instar in the disc proper of the wing disc survive.
Only 50% of homozygous clones generated at the early first larval instar in the peripodial epithelium of the wing disc survive, with most surviving near the disc stalk.
Homozygous clones generated at the second larval instar in the peripodial epithelium or disc proper of the wing disc both survive.
Homozygous clones in the eye disc (induced during the first larval instar) that span the margin cause either a delay in, or the inhibition of, retinal initiation.
Mutant clones in the distal parts of the leg are associated with tarsal segment fusions, as the joints fail to form within the mutant tissue. This joint loss is cell autonomous. In some cases where the mutant clone only forms a small part of the leg, no defects in segmentation are seen. In the proximal part of the leg, mutant clones are not associated with leg segment fusion, but rather with dark melanotic protrusions from the leg cuticle, which always occur near the site of an endogenous joint. Legs comprised almost entirely of mutant clone tissue (large clones induced using the Minute technique) show a failure of joint formation in segments extending from the tibia to tarsal segment 5, but proximal joints form normally.
Mutant embryos at stage 16 have hindguts about half the size of wild-type. These hindguts have larger lumens and two or three more cells in their circumference than those of wild-type. Hindguts are club shaped and smaller in both length and diameter. Hindgut epithelial cells are taller and narrower than seen in wild-type. The "boundary cells" that normally run the length of the large intestine are duplicated. Cell proliferation and apoptosis appear normal in mutant hindguts. Hindguts contain slightly fewer cells than wild-type. The visceral mesoderm is also normal in these mutants.
Homozygous embryos exhibit the 'tail-up' phenotype and defects in the mandible and maxilla. Hindgut is drastically reduced, proventriculus is absent. Second abdominal denticle belt is missing and the sixth abdominal denticle belt is defective in bowl1/bowl3 transheterozygotes. Lateralgraten is shortened and the ventral arm reduced in bowl1/bowl2 transheterozygotes.