Fig. 3. Src antagonizes E-cadherin during tracheal branching. (A-D) Dorsal branch morphologies in embryos with various levels of E-cadherin. Markers and genotypes are indicated on the left. (A) Control embryos carrying btl>GFP-moesin. Arrowhead indicates the lumen. L, length of dorsal branch (DB) measured and plotted in I and H. (B) Control embryos carrying btl>-catenin-GFP that labels the AJ as a black line in each dorsal branch. (C) In shg^IH/shg^E17B mutants, AJs became diffuse and discontinuous. (D) E-cadherin-GFP-expressing tracheae undergo slightly delayed, but morphologically normal, branching. Inset shows double lines of AJs remaining in the late stage of DB elongation. (E-H) Effect of activated Src42A on dorsal branch morphology and AJs. (E) In embryos expressing activated Src42A, tracheal cell contact persisted but became loose, and the lumen became discontinuous. (F) Src42A^ACT loosened AJs. Dotted circles indicate transiently detached cells at the tip of the DB. (G) This phenotype was further enhanced in the shg^IH/+ background. Most cells have now rounded up and lost accumulation of -catenin-GFP. (H) E-cadherin-GFP partially restored the extent of elongation of the DB and its lumen (compare with E). (I) Plot of the length of DBs (L, see A). The onset of DT fusion was set as time 0 for each measurement. When compared with DBs labeled with GFP-moesin, E-cadherin-GFP delayed DB elongation in an otherwise wild-type background. (J) E-cadherin-GFP partially restores elongation of DBs expressing Src42A^ACT. Original movies for A, C, D, E and H are presented as Movies 5-7 in the supplementary material. Scale bar in H: 25 µm.