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Fig. 4. sal acts upstream of svp during R3/R4 specification. All
panels represent third instar eye discs where svp–
clones (A-C, svpe22 – transcript null allele) or
sal– clones (D,E) were induced by Flipase-mediated
mitotic recombination and are labeled by the absence of ubi-GFP staining
(green). Anterior is to the left and the equator is at the top. The blue
channel shows ELAV. (A) Salm (red) expression in R3/R4 is not repressed after
row seven in the svp– area. In wild-type ommatidia,
Salm expression is progressively repressed in R3/R4 after row seven (arrows).
In svp– ommatidia, Salm expression persists in R3/R4
in more posterior rows (arrowheads). (B) In svp–
clones, Fmi (red) is present in all sides of the apical membrane of R3/R4
(arrowheads). In wild-type ommatidia, Fmi is localized in the equatorial side
of R3 and R4 (arrows). High magnification of svp–
(top, right) and wild-type (bottom, right) ommatidia (asterisk) show the
localization of Fmi in the R3 and R4 apical membrane (dashed line). (C) In
svp– clones, the expression of
m
0.5-lacZ (red) is lost in R4. (D) In
sal– ommatidia, sev-svp rescues
m0.5-lacZ (red) expression in one cell of the pair,
in many cases the one in the R4 position. In the wild-type ommatidia,
sev-svp leads to m0.5-lacZ expression in
both R3 and R4. (E) sev-Nact induces
m0.5-lacZ (red) in R3 and R4, both in
sal– and non-mutant ommatidia. Scale bars: 10
µm.
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