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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
shgIH/shgE17B 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) Src42AACT loosened
AJs. Dotted circles indicate transiently detached cells at the tip of the DB.
(G) This phenotype was further enhanced in the shgIH/+
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
Src42AACT. 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.
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