Fig. 7.

ApepP^EY embryos display Wnt activation phenotypes similar to Apc2 mutant embryos. (A-F) Anterior is to the left and posterior is to the right. (A-C′) Wild-type (A) and ApepP^EY mutant (B,C) cuticles. ApepP^EY cuticles exhibit head defects, fusion of the first and second denticle rows (compare A′ with B′, arrowhead) and denticle loss (B′, circled). ApepP^EY cuticles also have body holes (C,C′, circled). (D) Dose reduction of Apc2 in ApepP^EY embryos modifies the ApepP^EY phenotype. This example has head defects and denticle loss. (E,F) Wild-type (E) Arm protein localization and accumulation reflect patterned Wnt pathway activation, whereas ApepP^EY mutant embryos (F) exhibit a more uniform accumulation of Arm protein, as exemplified in the traces beneath. (G) 2D-DIGE comparison of wild-type and ApepP^EY embryos showing that total ApepP protein is decreased in mutant embryos and that there is a shift in isoform distribution toward the left isoform in ApepP^EY embryos. (H-J) Anti-Arm immunoblots of embryo lysates at 0-2 h (I) and 4-6 h (J) AEL. At 0-2 h AEL Arm significantly accumulates in both mutants, consistent with reduced Arm degradation, whereas at 4-6 h AEL Arm levels are decreased in both mutants (H; n=3 replicates).