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• W2013074640 abstract "The development of the multilayered cellular architecture found in many regions of the CNS requires axons originating in one layer or locale to terminate their growth with specificity in the layers that harbor their postsynaptic targets. In the developing chick visual system, for example, retinal ganglion cells of distinct subtypes send their axons to subtype-specific layers of the tectum (10Yamagata M. Sanes J.R. Development. 1995; 121: 3763-3776PubMed Google Scholar). A similar pattern of connectivity is found in the visual system of Drosophila, where photoreceptor axons, according to their cell type, terminate in either of two ganglion layers within the brain’s optic lobe. The six outer photoreceptors, R1–R6, of a single ommatidial unit of the fly compound eye terminate their axonal ingrowth within the brain’s most superficial layer, known as the lamina. The remaining two photoreceptors of an ommatidial unit, R7 and R8, extend beyond the lamina into a deeper layer known as the medulla. The specificity of outer photoreceptor axon termination in the lamina provides an attractive opportunity to elucidate the local mechanisms controlling a growth cone’s decision to stop or go. The eight axons from an ommatidial unit in the eye travel into the brain together as part of an ommatidium-specific fascicle (see the schematic diagram). Studies of photoreceptor axon elongation in larger insects reveal that transit along an ommatidial fascicle follows the temporal pattern of photoreceptor cell differentiation within the ommatidial unit in the eye (reviewed by 7Meinertzhagen, I.A., and Hanson, T.E. (1993). In The Development of Drosophila melanogaster, M. Bate and A. Martinez-Arias, eds. (Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press), pp. 1363–1491.Google Scholar). The growth cone from the initial R8 cell can be thought to pioneer the path to a retinotopic target destination, while the growth cones of R2 and R5, R3 and R4, R1 and R6, and R7 follow in sequence along the expanding ommatidial fiber. Whether the R8 axon is an essential pioneer for the fiber, and whether the other photoreceptor axonal types make the navigational decisions required of the R8 growth cone, is unclear. However, because the R8 axons grow into the deeper medulla layer, the R1–R6 growth cones must make the common decision to stop in the more superficial lamina layer. One could imagine a switch that terminates R1–R6 axonal extension, employing signals to which the R7 and R8 growth cones are blind. This is indeed an implication of the work reported in this issue of Neuron by 3Garrity P.A. Lee C.-H. Salecker I. Robertson H. Desai C. Zinn K. Zipursky S.L. Neuron. 1999; 22 (this issue): 707-717Abstract Full Text Full Text PDF PubMed Scopus (128) Google Scholar. Garrity et al. examine the role of the receptor protein tyrosine phosphatase PTP69D in photoreceptor axon pathfinding in Drosophila. Loss of PTP69D function in the retina results in a specific defect. The R1–R6 growth cones sometimes continue beyond their lamina termination point, following the paths of R7 and R8 axons into the deeper medulla layer. Further experiments demonstrate that an extracellular region harboring fibronectin-like motifs and at least one of the two intracellular phosphatase domains must be intact for PTP69D to function in lamina-specific termination. Presumably, upon ligand binding, PTP69D dephosphorylates substrates in the R1–R6 growth cones in order to terminate growth. The substrates that are dephosphorylated and the ligand involved remain to be determined. 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 neuromuscular connectivity (reviewed by 2Desai C.J. Sun Q. Zinn K. Curr. Opin. Neurobiol. 1997; 7 (b): 70-74Crossref PubMed Scopus (69) Google Scholar). These neural RPTPs are expressed on a subset of motor axons and growth cones. The motor neuron 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 nerve branch b (ISNb) motor axons sometimes fail to properly defasciculate from the intersegmental nerve (ISN) at the choice point leading to the ventrolateral muscle (VLM) field. The ISNb axons instead continue to grow dorsally, bypassing their VLM targets. This characteristic “bypass” phenotype is strongly enhanced by the additional loss of PTP69D function (1Desai C. Krueger N.X. Saito H. Zinn K. Development. 1997; 124 (a): 1941-1952Crossref PubMed Google Scholar), suggesting an overlap in the functional roles of PTP69D and Dlar at the ISNb choice point. What is the relationship of the neuromuscular RPTP mutant phenotypes to the behavior of R1–R6 growth cones in a Ptp69D mutant? One might view the visual system defect as a “bypass” of the R1–R6 axons’ lamina termination point. Blind to a lamina signal, the R1–R6 growth cones may fail to defasciculate from the R8 pioneer fiber. The observation that the majority of R1–R6 growth cones do stop in the lamina in a strong Ptp69D mutant background is consistent with the notion that other RPTPs, such as Dlar, contribute to proper R1–R6 termination. The answer to this question awaits the analysis of animals bearing multiple RPTP mutations. A deeper connection between RPTP activity and growth cone motility is suggested by the genetic and physical interactions of Dlar, the Abl tyrosine kinase, and the Abl substrate Enabled (Ena; 9Wills Z. Bateman J. Korey C.A. Comer A. Van Vactor D. Neuron. 1999; 22: 301-312Abstract Full Text Full Text PDF PubMed Scopus (262) Google Scholar; reviewed by 6Hu S. Reichardt L.F. Neuron. 1999; 22: 419-422Abstract Full Text Full Text PDF PubMed Scopus (31) Google Scholar). As with Dlar and Ptp69D, abl and ena loss of function yields defects in the dissociation of SNb motor axons from the ISN. Ena associates with the actin cytoskeleton at points of polymerization, where it may, via binding to profilin, modulate actin polymerization (see, for example, 4Gertler F.B. Niebuhr K. Reinhard M. Wehland J. Soriano P. Cell. 1996; 87: 227-239Abstract Full Text Full Text PDF PubMed Scopus (566) Google Scholar). The observation that Ena binds one of the intracellular phosphatase domains of PTP69D (9Wills Z. Bateman J. Korey C.A. Comer A. Van Vactor D. Neuron. 1999; 22: 301-312Abstract Full Text Full Text PDF PubMed Scopus (262) Google Scholar) suggests one possible connection between the reception of a lamina stop signal and the cytoskeletal events that control the motility of the R1–R6 growth cones. While the experiments of Garrity et al. implicate PTP69D in the R1–R6 growth cone’s initial decision to stop in the lamina, nitric oxide (NO) signal reception is apparently required to keep them there (5Gibbs S.M. Truman J.W. Neuron. 1998; 20: 83-93Abstract Full Text Full Text PDF PubMed Scopus (188) Google Scholar). NO is synthesized by lamina cells and can induce the synthesis of cGMP by the photoreceptor axons. Under pharmacological conditions that interfere with NO signaling, the R1–R6 growth cones initially stop in the lamina but later abandon the lamina and continue on further into the brain. The relative roles of these two signaling pathways in modulating R1–R6 growth cone motility is unclear. For example, it is not known whether the continued activity of PTP69D is required once the R1–R6 growth cones become dependent on NO to remain in the lamina. A further elaboration of the intersection between these two pathways in the modulation of growth cone motility would be an exciting avenue for future studies." @default.
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• W2013074640 title "Stop or Go in the Target Zone" @default.
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