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. Author manuscript; available in PMC: 2013 Nov 13.
Published in final edited form as: Nature. 2006 Mar 9;440(7081):10.1038/nature04615. doi: 10.1038/nature04615

Figure 3. spineless is sufficient to induce the yR7 fate.

Figure 3

a, Summary of the ss gain-of-function phenotype. All R7 cells adopt the yR7 fate (yellow); the fate of DRA ommatidia is unclear (grey). b, Water immersion microscopy on living wild-type flies expressing the yR7-specific reporter Rh4-GFP. Expression is restricted to one inner PR in a large subset of ommatidia. c, Rh4-driven GFP expression is dramatically expanded in LGMR>ss flies, as visualized by water immersion. d, In sGMR>ss flies, Rh4 (cyan) is expanded through the whole ss-overexpressing retina (compare with Fig. 1c). e, Rh4 (cyan) is completely lost in sev mutants, although Rh3 (red) is present in DRA R8 cells (arrow). f, Overexpression of ss (sGMR>ss) leads to ectopic Rh4 (cyan) in sev mutants. Rh3 (red) is restricted to DRA R8 cells (arrow). g, In whole-mount retinas from sGMR>ss flies, variegated expression of ss leads to the expansion of Rh4 (cyan) into a variable number of PRs per ommatidium; coexpression with Rh3 (red) is never observed (arrows). h, In wild-type eyes, the outer-PR opsin Rh1 (red) and Rh4 (cyan) never co-localize in the same PR cell. i, Ectopic expression of ss in sGMR>ss flies leads to massive expansion of Rh4 (cyan), with some co-localization (arrows) with the outer-PR opsin Rh1 (red).