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Fig. 6. RhoGAP Cv-c is localised basolaterally and controls Rho1 activity.
(A) Cuticles and distribution of GFP-Actin (green) in the spiracles of
wild-type and cv-c7 mutant embryos. Notice the partially
uninvaginated Filzkörpers in cv-c7 mutants (arrows)
accompanied by disruption of the apical Actin (inset). (B) Expression
of Venus-Cv-c (green) in spiracle cells using the ems-GAL4 driver, co-stained
with the basolateral marker 
-Spectrin (red) (i-iii) and with RhoGEF2
(red) (i'-iii'). (C) Cv-c gain of function (using emsGAL4
and UAS-Cv-c) leads to invagination failure of the most distal cells of the
spiracular chamber (arrowheads) correlating with a disruption of their apical
Actin (arrow). Green, GFP-Actin; red, Armadillo. (D) PKNG58AeGFP (i)
and mRFP-Actin (i') profiles in spiracles overexpressing RhoGAP Cv-c.
The cell cluster on the right (bracket) failed invagination and shows weaker
apical Rho1 activity (yellow arrowhead) than the remaining invaginated cells
(white arrowhead). (E) PKNG58AeGFP expression in a
cv-c7 mutant spiracle with a severe phenotype. Apical and
basal sections (dorsal view) and probe distribution along the xz axis. Notice
the apical restriction of active Rho1, non-uniformly associated with the
apical junctions. Scale bars: 10 µm.
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