Fig. 7. Genetic interaction between components of EGFR signaling pathway and DE-cadherin. (A-D) Cuticle preparations from wild-type and experimental embryos, all ventral views. (A) Wild-type embryo. (B) Shg^P34-1 homozygous embryos, head cuticle is missing but ventral trunk cuticle has relatively minor defects such as small holes in the cuticle (arrows). 12% of these cuticles have a more severe phenotype in which the entire ventral cuticle is missing, n=117. C: Da-GAL4; UAS-Activated EGFR; shg^P34–1/shg^P34–1, 27% of these embryos show lack of ventral cuticle, P=0.001, n=117, (arrows). (D) shg^P34–1/shg^P34–1;rho^M3/rho^M3. Among these double mutants, no embryos were observed that lacked the entire ventral cuticle. 8% of shg^P34–1/shg^P34–1 sibling embryos from this cross, lacked ventral cuticle, P=0.01, n=83. (E) Histogram of data.

Return to article