A Complex Sensory Map for Pheromones

cones sometimes continue beyond their lamina terminawith NO signaling, the R1–R6 growth cones initially stop tion point, following the paths of R7 and R8 axons into in the lamina but later abandon the lamina and continue the deeper medulla layer. Further experiments demonon further into the brain. The relative roles of these two strate that an extracellular region harboring fibronectinsignaling pathways in modulating R1–R6 growth cone like motifs and at least one of the two intracellular phosmotility is unclear. For example, it is not known whether phatase domains must be intact for PTP69D to function the continued activity of PTP69D is required once the in lamina-specific termination. Presumably, upon ligand R1–R6 growth cones become dependent on NO to rebinding, PTP69D dephosphorylates substrates in the main in the lamina. A further elaboration of the intersecR1–R6 growth cones in order to terminate growth. The tion between these two pathways in the modulation of substrates that are dephosphorylated and the ligand growth cone motility would be an exciting avenue for involved remain to be determined. future studies. PTP69D, like two other Drosophila receptor tyrosine phosphatases (RPTPs), Dlar and PTP99A, is in the collection of molecules with a role in the establishment of Samuel Kunes neuromuscular connectivity (reviewed by Desai et al., Department of Molecular and Cellular Biology 1997b). These neural RPTPs are expressed on a subset Harvard University of motor axons and growth cones. The motor neuron Cambridge, Massachusetts 02138 pathfinding defects in animals harboring one or multiple RPTP mutations are typically a stall or miscue at particular choice points. In Dlar mutants, the intersegmental Selected Reading nerve branch b (ISNb) motor axons sometimes fail to properly defasciculate from the intersegmental nerve Desai, C., Krueger, N.X., Saito, H., and Zinn, K. (1997a). Development 124, 1941–1952. (ISN) at the choice point leading to the ventrolateral muscle (VLM) field. The ISNb axons instead continue to Desai, C.J., Sun, Q., and Zinn, K. (1997b). Curr. Opin. Neurobiol. 7, 70–74. grow dorsally, bypassing their VLM targets. This characteristic “bypass” phenotype is strongly enhanced by the Garrity, P.A., Lee, C.-H., Salecker, I., Robertson, H., Desai, C., Zinn, K., and Zipursky, S.L. (1999). Neuron 22, this issue, 707–717. additional loss of PTP69D function (Desai et al., 1997a),