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Fig. 7. Dsh is not required for dorsal closure to proceed when the `canonical' Wg
pathway is activated. Cuticles (A-C'), Fmi (green) and Dlg (red)
antibody staining (A''-C'') of dshGLC
(A-A''), dshGLC>da>Dsh (B-B'') and
sgg,dshGLC (C-C'') embryos. The cuticle of
dshGLC embryos presents an anterodorsal hole (A',
arrowheads) and is very short with most of the dorsal epidermis missing (A).
In dshGLC>da>Dsh embryos, the length and the hole of
the cuticle are rescued (B) and a strong puckering is now observed dorsally
(B'). The cell morphology and polarity in dshGLC
embryos is very similar to that observed in wg–
embryos (compare A'' with Fig.
1B): the DME cells are stretched in the AP direction while the
other dorsal epidermal cells present a rather isotropic shape. Fmi does not
localise at the membrane but shows a `dotty' localisation in the epidermis.
Upon ubiquitous overexpression of Dsh in dshGLC, the DME
cells elongation in the DV direction is rescued (B''). Fmi does not
localise at the membrane in stage 13 embryos (not shown), but shows membrane
localisation and ANCs accumulation in late stage 13-early stage 14 embryos
(B''). The cuticle of sgg,dshGLC embryos (C), which
lacks both dsh and sgg function, presents a strong
retraction defect and a ventral naked cuticle characteristic of the
constitutive activation of the `canonical' Wg pathway associated with the loss
of sgg function. They present an anterior hole (arrowhead) and a
puckering of the dorsal midline (C'). Although the retraction defect
makes the observations difficult, the cuticle is longer than in
dshGLC embryos (compare with A). Fmi localises at the
membrane and concentrates at ANCs in sgg,dshGLC embryos
(C'') and the main direction of DME cells is restored to the DV axis.
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