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Fig. 3. Overexpression of Roe phenocopies N loss-of-function phenotypes
and represses N target genes during eye development.
(A,A') roe overexpression clones (marked by GFP
in green, outlined in A') in third instar eye disc cause recruitment of
supernumerary photoreceptors (anti-Elav, magenta), similar to N pathway
loss-of-function clones (compare with Fig.
5E). (B) Tangential section of adult eye of the genotype
sepGAL4, UAS-roe with schematic shown on the right (black
and red arrows represent the two chiral forms; green arrows represent
symmetrical clusters; black dot shows loss of R cells). Increased levels of
Roe expression in R3/R4 precursors often cause the formation of symmetrical
R3/R3 type ommatidia (some R4/R4 type are also observed; quantified in C).
(C) Quantification of the phenotypes of sev-driven expression
of roe, N
ECD and together. Ectopic
expression of NECD causes a high number of R4/R4-type
symmetrical ommatidia and R-cell loss, while Roe causes mostly R3/R3-type and
occasional R-cell loss. The NECD phenotype is antagonized by
Roe co-expression and a reversion to a significant percentage of R3/R3-type
ommatidia typical of Roe overexpression is observed (the `loss of R-cell'
phenotype is enhanced, see text for details). Total number of ommatidia scored
was 391 (roe), 545 (NECD) and 329
(roe + NECD) with at least three
eyes per genotype analyzed. (D,D') Third instar eye disc
bearing clones of cells expressing two copies of sepGAL4,
UAS-roe (marked by absence of Ubi-GFP in green, see Materials
and methods). Expression of the R4-specific N reporter
m
-lacZ (red) is largely suppressed inside the
Roe-overexpressing tissue. Cells outside the clone can be either wild type or
have one copy of sepGAL4, UAS-roe, which can also suppress
m-lacZ to a lower extent (not shown). 
-Elav is
in blue.
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