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Published April 1999 | Published
Journal Article Open

The Drosophila SH2-SH3 adapter protein Dock is expressed in embryonic axons and facilitates synapse formation by the RP3 motoneuron


The Dock SH2-SH3 domain adapter protein, a homolog of the mammalian Nck oncoprotein, is required for axon guidance and target recognition by photoreceptor axons in Drosophila larvae. Here we show that Dock is widely expressed in neurons and at muscle attachment sites in the embryo, and that this expression pattern has both maternal and zygotic components. In motoneurons, Dock is concentrated in growth cones. Loss of zygotic dock function causes a selective delay in synapse formation by the RP3 motoneuron at the cleft between muscles 7 and 6. These muscles often completely lack innervation in late stage 16 dock mutant embryos. RP3 does form a synapse later in development, however, because muscles 7 and 6 are normally innervated in third-instar mutant larvae. The absence of zygotically expressed Dock also results in subtle defects in a longitudinal axon pathway in the embryonic central nervous system. Concomitant loss of both maternally and zygotically derived Dock dramatically enhances these central nervous system defects, but does not increase the delay in RP3 synaptogenesis. These results indicate that Dock facilitates synapse formation by the RP3 motoneuron and is also required for guidance of some interneuronal axons The involvement of Dock in the conversion of the RP3 growth cone into a presynaptic terminal may reflect a role for Dock-mediated signaling in remodeling of the growth cone's cytoskeleton.

Additional Information

© 1999 The Company of Biologists Limited. Accepted 13 January; published on WWW 3 March 1999. We thank Jim Clemens, Jack Dixon and Mark Perin for antibodies, the Bloomington Stock Center and Corey Goodman's group for fly strains, and Steven Hanks and Richard Kim for helpful advice. This work was supported by NIH R01 grant NS28182 to K. Z., by startup funds from Vanderbilt University Medical School to C. J. D. and by NIH R01 grant NS31651 to H. K.; P. A. G. was supported by postdoctoral fellowships from the Bank of America-Giannini Foundation and the Leukemia Society of America; S. L. Z. is an Investigator of the Howard Hughes Medical Institute.

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