The receptor tyrosine phosphatase DLAR controls R7 axon targeting in the Drosophila visual system. T. Suzuki ¹, C. Maurel-Zaffran ², G. Gahmon ¹, B.J. Dickson ¹, J.E. Treisman ². 1) Research Institute of Molecular Pathology, Vienna, Austria; 2) Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York.

   In the adult Drosophila visual system, axons of the R1-R6, R7 and R8 photoreceptors target different layers in the optic lobe: R1-R6 axons terminate in the lamina, R7 and R8 in different layers of the medulla. We have performed large scale genetic screens of eye-specific mosaics, seeking to identify mutations that disrupt this pattern of axon targeting. In one complementation group, represented by 5 alleles, most of all R7 axons mistarget the R8 layer of the medulla. R1-R6 and R8 axons terminate in their normal layers. These alleles were found to all carry mutations in the DLAR gene, which encodes a receptor tyrosine phosphatase previously shown to regulate axon fasciculation in the Drosophila embryo. As in the embryo, the DLAR mutant phenotype in the eye is suppressed by either increasing Ena levels or decreasing Abl levels, suggesting that the downstream signalling pathways are the same in both systems. DLAR is strongly expressed on R7, R8 photoreceptor axons and in medulla cortex. R7 targeting defect in DLAR mosaic is rescued by expression of UAS-DLAR under the sevenless (sev)-GAL4, indicating that DLAR is autonomously required in R7 phtoreceptor neurons. T.S. and C. M-Z contributed equally.