The third midgut chamber is greatly reduced in size in homozygous embryos. The central and posterior constrictions that form this chamber form normally, but are located more closely together than in the wild-type gut. 85% of embryos fail to form the anterior constriction completely; the constriction initiates at its normal site but does not significantly constrict the midgut. Elongation of gastric caecae is not seen in these embryos. The number of visceral mesoderm (VM) cells in the third midgut chamber is reduced compared to wild-type, while the first, second and fourth midgut chambers contain normal numbers of cells. Defects in VM cell segregation are seen immediately after the stage 12 mitosis, producing a junction in the central midgut. By stage 16, VM cells are often scattered around the surface of the midgut, in contrast to the ordered files of cells seen in wild-type embryos.

pnt²/pnt^Δ88 embryos exhibit subtle ventral defects. Leg and eye/antenna pnt²/pnt^Δ88 mutant discs can be in vivo cultured. Wing and haltere discs cannot.

Mutation has no effect on rho^hs.sev rough eye phenotype.

Nondefective in gonad assembly.

Tracheal dorsal trunks fail to form in the embryo, due to failure in migration of trachea cells. Embryonic muscles 4, 11, 19 and 20 are absent and muscles 15, 16 and 17 are small and displaced (though note that the ventral epidermis is affected in pnt mutants). Commissures in the CNS are fused.

Salivary placodes are expanded towards the ventral midline.

Enhancement of tor^13D embryos: decrease in proportion of embryos that formed cuticle, or cuticle with denticles and increase in proportion of embryos that formed empty sacs.