Fig. 6. Genetic interaction of Rac and FGF signaling. (A-C) Phenotypes of embryos deficient in Rac and FGF signaling classified into three classes. Rac1, 2/Rac1, 2 (A, mild), Rac1, 2/Rac1, 2 (B, intermediate) and Rac1, 2/bnl^P1 laid by Rac1, 2/+ mother (C, severe) were stained with monoclonal antibody 2A12 to label the tracheal lumen. In Rac1, 2 mutants, the DT is disrupted (A,B) with a defect in germband retraction (arrow in B). In Rac1, 2/bnl^P1 mutants, no tracheal cell migration has taken place (C). (D,E) Partial rescue of the btl mutant phenotype by the expression of the constitutively active form of Rac1. (D) A btl^Oh10 mutant embryo at stage 12. Tracheal cells are labeled with a nuclear ß-galactosidase marker. No sign of branching is apparent. (E) A btl^Oh10 mutant embryo at stage 12 expressing Rac1V12 by the btl enhancer. GFP-moesin and dp-MAPK are shown in green and purple, respectively. Tracheal cells were able to move. (F) Genetic interactions involving Rac. Maternal and zygotic genotypes of scored embryos are indicated. Tracheal phenotypes were classified into `normal' (white bar), `weak' (yellow bar) and `intermediate' (blue bar), according to the number of truncated DT of none, one to three, and four to nine, respectively, per one side of embryos. The `severe' class (red bar) corresponds to the phenotype of no tracheal migration at all. `n' is the number of embryos observed. Scale bars: in A, 40 µm for A-C; in D, 20 µm for D,E.

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