Inhibition of FGF Receptor Activity in Retinal Ganglion Cell Axons Causes Errors in Target Recognition

McFarlane, Sarah; Cornel, Elsa; Amaya, Enrique; Holt, Christine

doi:10.1016/s0896-6273(00)80156-7

Cited by 142 publications

(126 citation statements)

References 48 publications

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“…Eyes from the embryos electroporated with GFP-or CA-Rab5c were cultured overnight in basal medium on polylysine/ laminin substrata, and the elongation rate was measured by time-lapse recording. The extension rate of GFP-expressing axons was 35 Ϯ 1.4 m/h (N ϭ 400), a value close to that previously reported for RGC axons in vitro (McFarlane et al, 1996). Consistent with the effect of primaquine, the extension rate of axons expressing Xenopus CA-Rab5c dropped by 33%.…”

Section: Constitutively Active Rab5 Impairs Axon Extension In Vitrosupporting

confidence: 88%

Rab5 and Rab4 Regulate Axon Elongation in theXenopusVisual System

et al. 2014

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The elongation rate of axons is tightly regulated during development. Recycling of the plasma membrane is known to regulate axon extension; however, the specific molecules involved in recycling within the growth cone have not been fully characterized. Here, we investigated whether the small GTPases Rab4 and Rab5 involved in short-loop recycling regulate the extension of Xenopus retinal axons. We report that, in growth cones, Rab5 and Rab4 proteins localize to endosomes, which accumulate markers that are constitutively recycled. Fluorescence recovery after photo-bleaching experiments showed that Rab5 and Rab4 are recruited to endosomes in the growth cone, suggesting that they control recycling locally. Dynamic image analysis revealed that Rab4-positive carriers can bud off from Rab5 endosomes and move to the periphery of the growth cone, suggesting that both Rab5 and Rab4 contribute to recycling within the growth cone. Inhibition of Rab4 function with dominant-negative Rab4 or Rab4 morpholino and constitutive activation of Rab5 decreases the elongation of retinal axons in vitro and in vivo, but, unexpectedly, does not disrupt axon pathfinding. Thus, Rab5-and Rab4-mediated control of endosome trafficking appears to be crucial for axon growth. Collectively, our results suggest that recycling from Rab5-positive endosomes via Rab4 occurs within the growth cone and thereby supports axon elongation.

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Section: Constitutively Active Rab5 Impairs Axon Extension In Vitrosupporting

confidence: 88%

Rab5 and Rab4 Regulate Axon Elongation in theXenopusVisual System

et al. 2014

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“…Although slits could be the ADAM10 target in the mid-diencephalon, they are unlikely to be the molecular substrate at the optic tectum because no defects were observed in target innervation in the mouse mutants. One possible cleavage substrate at the tectum is suggested by the similarity of the target recognition phenotype seen with ADAM10 inhibition and disruption of fibroblast growth factor signaling (McFarlane et al, 1995(McFarlane et al, , 1996Walz et al, 1997). Alternatively, two recent studies suggest that the secreted Tlr (Tolloid-related) metalloproteinase functions in the recognition of muscle targets by Drosophila motor axons by promoting defasciculation of axons from the motor nerve in the vicinity of the target (Meyer and Aberle, 2006;Serpe and O'Connor, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…CS2GFP or CS2DNXadam10-mt was mixed with the cationic transfection agent N- [1-(2,3-dioleoyloxyl)propyl]-N, N, N-trimethylammoniummethyl sulfate (DOTAP; Roche) in a 3:1 w/v DNA/DOTAP ratio. The mixture was loaded into a fine-pulled micropipette and pressure injected into the developing eye primordium by using a Picospritzer II (Holt et al, 1990;McFarlane et al, 1996). Embryos were processed for whole-mount immunochemistry with antibodies against GFP and myc.…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, to investigate a role for ADAM10 in vertebrate axon guidance in vivo, we used the developing retinotectal projection of the frog Xenopus laevis as our model. The visual system has been well characterized, development occurs rapidly, and several approaches are available to investigate the roles of specific molecules in the guidance of the retinal ganglion cell (RGC) axons (Chien et al, 1993;McFarlane et al, 1996;Haas et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…As a result, RGC axons likely join other axons growing in the tracts running alongside the border of the optic tectum, the tract of the posterior commissure, and the tract of the posterior optic commissure (McFarlane et al, 1996). ADAM10 also appears to be required for RGC axon guidance at a caudal turn in the mid-diencephalon.…”

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confidence: 99%

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Targeting of Retinal Axons Requires the Metalloproteinase ADAM10

Chen

Hehr²,

Atkinson‐Leadbeater³

et al. 2007

J. Neurosci.

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The role of extrinsic cues in guiding developing axons is well established; however, the means by which the activity of these extrinsic cues is regulated is poorly understood. A disintegrin and metalloproteinase (ADAM) enzymes are Zn-dependent proteinases that can cleave guidance cues or their receptors in vitro. Here, we identify the first example of a metalloproteinase that functions in vertebrate axon guidance in vivo. Specifically, ADAM10 is required for formation of the optic projection by Xenopus retinal ganglion cell (RGC) axons. Xadam10 mRNA is expressed in the dorsal neuroepithelium through which RGC axons extend. Pharmacological or molecular inhibition of ADAM10 within the brain each resulted in a failure of RGC axons to recognize their target. In contrast, molecular inhibition of ADAM10 within the RGC axons themselves had no effect. These data argue strongly that in the dorsal brain ADAM10 acts cell non-autonomously to regulate the guidance of RGC axons.

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Degeneration and regeneration of ganglion cell axons

Weise¹,

Ankerhold²,

Bähr³

2000

Microsc. Res. Tech.

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The retino‐tectal system has been used to study developmental aspects of axon growth, synapse formation and the establishment of a precise topographic order as well as degeneration and regeneration of adult retinal ganglion cell (RGC) axons after axonal lesion. This paper reviews some novel findings that provide new insights into the mechanisms of developmental RGC axon growth, pathfinding, and target formation. It also focusses on the cellular and molecular cascades that underlie RGC degeneration following an axonal lesion and on some therapeutic strategies to enhance survival of axotomized RGCs in vivo. In addition, this review deals with problems related to the induction of regeneration after axonal lesion in the adult CNS using the retino‐tectal system as model. Different therapeutic approaches to promote RGC regeneration and requirements for specific target formation of regenerating RGCs in vitro and in vivo are discussed. Microsc. Res. Tech. 48:55–62, 2000. © 2000 Wiley‐Liss, Inc.

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Inhibition of FGF Receptor Activity in Retinal Ganglion Cell Axons Causes Errors in Target Recognition

Cited by 142 publications

References 48 publications

Rab5 and Rab4 Regulate Axon Elongation in theXenopusVisual System

Rab5 and Rab4 Regulate Axon Elongation in theXenopusVisual System

Targeting of Retinal Axons Requires the Metalloproteinase ADAM10

Degeneration and regeneration of ganglion cell axons

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