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Published April 1999 | public
Journal Article

Retinal Axon Target Selection in Drosophila Is Regulated by a Receptor Protein Tyrosine Phosphatase

Abstract

Different Drosophila photoreceptors (R cells) connect to neurons in different optic lobe layers. R1–R6 axons project to the lamina; R7 and R8 axons project to separate layers of the medulla. We show a receptor tyrosine phosphatase, PTP69D, is required for lamina target specificity. In Ptp69D mutants, R1–R6 project through the lamina, terminating in the medulla. Genetic mosaics, transgene rescue, and immunolocalization indicate PTP69D functions in R1–R6 growth cones. PTP69D overexpression in R7 and R8 does not respecify their connections, suggesting PTP69D acts in combination with other factors to determine target specificity. Structure–function analysis indicates the extracellular fibronectin type III domains and intracellular phosphatase activity are required for targeting. We propose PTP69D promotes R1–R6 targeting in response to extracellular signals by dephosphorylating substrate(s) in R1–R6 growth cones.

Additional Information

© 1999 by Cell Press. Received 25 January 1999, Revised 26 February 1999, Available online 22 September 2000. We thank Ulrike Gaul ror providing Ro-lacZ^(tau) flies and Christian Klaembt for gal4 line 1.3 02 prior to publication. The authors thank the members of the Zipursky laboratory, Andreas Bergmann, Frank Gertler, Linda Huang. and Hermann Steller for comments on the manuscript and helpful discussion. P. A. G. has been supported by a Helen Hay Whitney Postdoctoral Fellowship, a Bank of America Giannini Foundation Medical Research Fellowship, a Leukemia Society of America Special Fellowship, a McKnight Endowment Fund for Neuroscience Scholar Award, and startup funds from the Massachusetts Institute of Technology. C.-H. L. is a Howard Hughes Medical Institute Fellow of the life Sciences Research Foundation. I. S. has been supported by a fellowship of Deutsche Forschungsgemeinschaft and by the Howard Hughes Medical Institute. K. Z. and C. J. D. were supported by NIH RO1 grant NS28182. S. L. Z. is an Investigator of the Howard Hughes Medical Institute. H. C. R. was supported by NIH predoctoral training grant 5 T32 GM072B7-24.

Additional details

Created:
August 19, 2023
Modified:
October 25, 2023