Fig. 4. Reduction in Apc1 enhances ectopic Wg transduction in the Apc2 mutant. (A-C) Cuticles of embryos from Apc2^d40/Apc2^d40 mothers and Apc2^d40 fathers (A); Apc1^Q8Apc2^d40/Apc2^d40 mothers and Apc2^d40 fathers (B); Apc2^d40/Apc2^d40 mothers and Apc1^Q8 Apc2^d40 fathers (C). Most of the denticles that remain in Apc2^d40 mutants are eliminated by reducing the maternal or zygotic dose of Apc1 by half. (D-I) Embryos from Apc1^Q8 Apc2^d40 germline clones, which lack maternally provided wild-type Apc1 and Apc2. Cuticles (D-F) and Engrailed stripes (G-I) in embryos from Apc1^Q8 Apc2^d40 germline clones with a wild-type zygotic allele of Apc1 and Apc2 (D,G), Apc1^Q8 Apc2^d40 germline clone embryo homozygous for only Apc2^d40 (E,H) or homozygous for only Apc1^Q8 (F,I). The ectopic Wg activation caused by simultaneous homozygous reduction of Apc1 and Apc2 maternally is made more severe by elimination of either zygotic wild-type Apc1 or zygotic wild-type Apc2. (J) A quantitative analysis of embryonic cuticular patterning defects that result from the Apc1^Q8 and Apc2^d40 mutations.

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