Fig. 3. Reduction in Egfr signaling affects ommatidial rotation. Panels show tangential adult eye sections around the equator and corresponding schemes reflecting ommatidial rotation. Orientation and arrows are as in Fig. 1, `circles' represent ommatidia with loss of photoreceptors that cannot be unambiguously scored (`asterisk' indicates the rare event of a symmetrical ommatidium). (A) Egfr^top1/Egfr^top1, (B) Egfr^top1/Egfr^topEC20. The hypomorphic Egfr^top1 allele and Egfr^top1/Egfr^EC20 allelic combination show typical rotation defects. Reduction of Egfr activity in Star^–/+ causes rotation defects and is dominantly enhanced by components of Egfr signaling. Star is haplo-insufficient for eye development (note rare photoreceptor loss and rotation defects). The rotation defects are dominantly enhanced by removal of components of the Egfr/Ras pathway (compare C with D,E). Note that canoe, flamingo and zipper heterozygosity also enhances the S^–/+ phenotype (see Table 1 for other genotypes and quantification). (C) S^48-5/+, (D) S^48-5/+, Egfr^top1/+, (E) S^48-5/+; ras1^e2F/+, (F) S^48-5/+; cno²/+, (G) S^48-5/+; fmi^E59/+, (H) S^48-5/+; zipper⁰²⁹⁵⁷/+.

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