Polarizing membrane dynamics and adhesion for growth cone navigation

Itofusa, Rurika; Kamiguchi, Hiroyuki

doi:10.1016/j.mcn.2011.03.007

Cited by 30 publications

(23 citation statements)

References 80 publications

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“…During development the endocytosis of receptors and their ligands is an important signaling mechanism, which promotes neuronal differentiation, migration, neuritogenesis and outgrowth, and axon guidance (Itofusa, 2011; Kawauchi, 2012; Tian et al, 2012; Zhang et al, 2000). Pharmacological inhibition of endocytosis increases surface localization of FGFR1 and increases FGF2-dependent axon branching, suggesting that basal endocytosis of the receptor reduces FGF dependent axon branching (Hausott et al, 2011).…”

Section: Endocytosismentioning

confidence: 99%

Membrane Trafficking in Neuronal Development: Ins and Outs of Neural Connectivity

Winkle

Gupton

2016

International Review of Cell and Molecular Biology

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During development, neurons progress through rapid yet stereotypical shape changes to achieve proper neuronal connectivity. This morphological progression requires carefully orchestrated plasma membrane expansion, insertion of membrane components including receptors for extracellular cues into the plasma membrane and removal and trafficking of membrane materials and proteins to specific locations. This review outlines the cellular machinery of membrane trafficking that play an integral role in neuronal cell shape change and function from initial neurite formation to pathway navigation and synaptogenesis.

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Section: Endocytosismentioning

confidence: 99%

Membrane Trafficking in Neuronal Development: Ins and Outs of Neural Connectivity

Winkle

Gupton

2016

International Review of Cell and Molecular Biology

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“…This sequence can be phosphorylated by pp60 c-src on Tyr 1176 (Schaefer et al, 2002), and is important for AP2/clathrin-mediated endocytosis and axonal trafficking (Kamiguchi and Lemmon, 1998; Kamiguchi et al, 1998; Wisco et al, 2003) during growth cone navigation (Itofusa and Kamiguchi, 2011). ERMs mediate L1-induced axon branching (Cheng et al, 2005) and guidance (Mintz et al, 2008), as well as Semaphorin3A-induced growth cone collapse (Mintz et al, 2008; Schlatter et al, 2008).…”

Section: Resultsmentioning

confidence: 99%

EphB regulates L1 phosphorylation during retinocollicular mapping

Dai

Dalal

Thakar

et al. 2012

Molecular and Cellular Neuroscience

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Interaction of the cell adhesion molecule L1 with the cytoskeletal adaptor ankyrin is essential for topographic mapping of retinal ganglion cell (RGC) axons to synaptic targets in the superior colliculus (SC). Mice mutated in the L1 ankyrin-binding motif (FIGQY1229H) display abnormal mapping of RGC axons along the mediolateral axis of the SC, resembling mouse mutant phenotypes in EphB receptor tyrosine kinases. To investigate whether L1 functionally interacts with EphBs, we investigated the role of EphB kinases in phosphorylating L1 using a phospho-specific antibody to the tyrosine phosphorylated FIGQY1229 motif. EphB2, but not an EphB2 kinase dead mutant, induced tyrosine phosphorylation of L1 at FIGQY1229 and perturbed ankyrin recruitment to the membrane in L1-transfected HEK293 cells. Src family kinases mediated L1 phosphorylation at FIGQY1229 by EphB2. Other EphB receptors that regulate medial-lateral retinocollicular mapping, EphB1 and EphB3, also mediated phosphorylation of L1 at FIGQY1229. Tyrosine1176 in the cytoplasmic domain of L1, which regulates AP2/clathrin-mediated endocytosis and axonal trafficking, was not phosphorylated by EphB2. Accordingly mutation of Tyr1176 to Ala in L1-Y1176A knock-in mice resulted in normal retinocollicular mapping of ventral RGC axons. Immunostaining of the mouse SC during retinotopic mapping showed that L1 colocalized with phospho-FIGQY in RGC axons in retinorecipient layers. Immunoblotting of SC lysates confirmed that L1 was phosphorylated at FIGQY1229 in wild type but not L1-FIGQY1229H (L1Y1229H) mutant SC, and that L1 phosphorylation was decreased in the EphB2/B3 mutant SC. Inhibition of ankyrin binding in L1Y1229H mutant RGCs resulted in increased neurite outgrowth compared to WT RGCs in retinal explant cultures, suggesting that L1-ankyrin binding serves to constrain RGC axon growth. These findings are consistent with a model in which EphB kinases phosphorylate L1 at FIGQY1229 in retinal axons to modulate L1-ankyrin binding important for mediolateral retinocollicular topography.

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“…Increasing evidences show that axon guidance is indeed related with changes in intracellular calcium concentration. Tojima and colleagues clearly demonstrated that calcium is important for growth cone attraction in chick DRG neurons [11], [41] and several studies showed that intracellular Ca 2+ stores are important for axon navigation [42]–[44]. It is still under debate whether Semaphorin guidance cues also require calcium signaling to trigger repulsive guidance effects.…”

Section: Discussionmentioning

confidence: 99%

R-Type Calcium Channels Are Crucial for Semaphorin 3A–Induced DRG Axon Growth Cone Collapse

Treinys

Kaselis

Jover³

et al. 2014

PLoS ONE

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Semaphorin 3A (Sema3A) is a secreted protein involved in axon path-finding during nervous system development. Calcium signaling plays an important role during axonal growth in response to different guidance cues; however it remains unclear whether this is also the case for Sema3A. In this study we used intracellular calcium imaging to figure out whether Sema3A-induced growth cone collapse is a Ca2+ dependent process. Intracellular Ca2+ imaging results using Fura-2 AM showed Ca2+ increase in E15 mice dorsal root ganglia neurons upon Sema3A treatment. Consequently we analyzed Sema3A effect on growth cones after blocking or modifying intracellular and extracellular Ca2+ channels that are expressed in E15 mouse embryos. Our results demonstrate that Sema3A increased growth cone collapse rate is blocked by the non-selective R- and T- type Ca2+ channel blocker NiCl2 and by the selective R-type Ca2+ channel blocker SNX482. These Ca2+ channel blockers consistently decreased the Sema3A-induced intracellular Ca2+ concentration elevation. Overall, our results demonstrate that Sema3A-induced growth cone collapses are intimately related with increase in intracellular calcium concentration mediated by R-type calcium channels.

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Polarizing membrane dynamics and adhesion for growth cone navigation

Cited by 30 publications

References 80 publications

Membrane Trafficking in Neuronal Development: Ins and Outs of Neural Connectivity

Membrane Trafficking in Neuronal Development: Ins and Outs of Neural Connectivity

EphB regulates L1 phosphorylation during retinocollicular mapping

R-Type Calcium Channels Are Crucial for Semaphorin 3A–Induced DRG Axon Growth Cone Collapse

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