12% of Apc2N175K maternally mutant syncytial embryos show movement of over 2% of cortical nuclei into the embryo interior, compared to 0-3% of wild-type embryos.
The cuticle of an average Apc2N175K maternal/zygotic embryo shows an anterior hole, is 50-60% the length of wild-type and has 3 patches of denticles remaining.
Homozygous flies have wing vein and bristle defects and slightly rough eyes. Mutant females lay very few eggs and only some of these eggs develop through late embryonic stages. These escaper embryos produce cuticles that are completely naked on the ventral side. Ovaries of homozygous females contain very few mature egg chambers and oocytes are often underdeveloped in large chambers. The nurse cells tend to be irregularly arranged within maturing egg chambers. In 17% of egg chambers, the oocyte is mispositioned to one side of the anterior-posterior axis, rather than occupying the most posterior position of the egg chamber as in wild type. Mutant egg chambers have fewer membrane stacks in the plasma membranes of the germ cells than wild type, or abnormal stacks, showing long stretches of thin straight membrane interfaces that are devoid of membrane interdigitations. Cell vertices and ring canals also contain fewer membrane stacks than normal or abnormal membrane stacks, tending to have a flimsy appearance. There are numerous gaps between nurse cell membranes, especially at three-cell joins, the most abnormal of which have gaping holes. The number of spot adherens junctions is reduced to 31% of wild type in the epithelial cells of stage 6/7 embryos derived from Apc2N175K parents. These embryos have extensive gaps between the lateral plasma membranes and large gaping holes at three-cell joins.
Apc2 alleles can be divided into three categories based on their embryonic cuticle phenotypes, from weak to moderate to strong: Apc2e90 = Apc2b5 = Apc2N175K < Apc2c9 = Apc2ΔS = Apc2d40 < Apc2g41 = Apc2f90 = Apc2g10.