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Fig. 1. The effect of otk mutations on R-cell projection pattern at larval stage. All R-cell axons in third-instar larvae (A,B) were stained with MAb 24B10. R2-R5 axons in third-instar larvae (C-F) were labeled with the larval R2-R5 marker ro--lacZ. In wild type (A), after exiting the optic stalk (os), R7 and R8 growth cones passed through the lamina into the medulla, whereas R1-R6 growth cones stop within the lamina, which could be identified as a continuous line of MAb 24B10 immunoreactivity. In B, an otk³ mosaic individual in which 80-90% eye tissues were homozygous otk³ mutant ommatidia, displayed defects in R-cell projections. The lamina plexus was uneven with the presence of small gaps. Abnormal thicker bundles were observed within the medulla. In wild type (C), ro--lacZ labeled R2-R5 axons terminated within the lamina. In an otk³ mosaic individual (D), many labeled R2-R5 axons projected aberrantly into the medulla. Similar mistargeting phenotype was also observed in otk³/otk^EP(2)2017 transheterozygous larvae (E). In an otk³/otk^EP(2)2017 transheterozygous larvae expressing an UAS-otk transgene in R cells under control of the GMR-GAL4 driver (Mismer and Rubin, 1987) (F), most labeled R2-R5 axons now terminated within the lamina. Scale bar: 20 µm.

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