Figure 5. Genetically lowering kirre dosage in the RTW6 revertant causes defects in adult ommatidial organization.

(A) Scanning electron micrographs. Compound eye phenotype from a RTW6/Df(1)w^67k30 heterozygote female, compared to those from her parent genotypes, RTW6/Y and Df((1)w^67k30)/+. Leaving only the kirre copy present in the RTW6 chromosome when no functional copies of rst are present in the eye lead to a mild but clear disruption of ommatidial patterning showed in the inset: lack or mispositioning of mechanosensory bristles (arrowheads), bristle duplications (arrow) and fused ommatidia (asterisk). (B) Dissecting stereomicroscope images. Head from a RTW6 male where kirre function has been almost completely knocked down by expressing one copy of the UAS-kirre RNAi 3111 transgene under the control of the GMR-Gal4 eye driver (see methods). Eyes from a male carrying only the driver and a RWT6/Y are also shown. Note the clear increase in the severity of the phenotype, particularly the higher number of fused ommatidia and mispositioned bristles, compared to the RTW6/Df(1)w^67k30eye in (A).