The endogenous Apc promoter drives expression of a mutated form of Apc2 : two of the conserved Ser residues in the potential GSK3 phosphorylation site of region B have been mutated to Ala, preventing phosphorylation at these residues.
The embryonic lethality along with cuticle defects (loss of denticles, expansion of naked cuticle) characteristic for maternal/zygotic Apc2g10,ApcQ8 mutants is only weakly rescued by combination with Apc2AA.