Semaphorin 3A induces CaV2.3 channel-dependent conversion of axons to dendrites

Nishiyama, Makoto; Togashi, Kazunobu; Schimmelmann, Melanie J. von; Lim, Chae‐Seok; Maeda, Satoshi; Yamashita, Naoya; Goshima, Yoshio; Ishii, Shin; Hong, Kiryong

doi:10.1038/ncb2255

Cited by 46 publications

(43 citation statements)

References 50 publications

(72 reference statements)

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“…1). This result indicates that nimodipine-sensitive Ca 2+ channels, including R-type Ca 2+ channel, mediate Sema3A-induced colocalization of PlexA4 and TrkA in both growth cones and axons (Nishiyama et al, 2011;Treinys et al, 2014). MDC also suppressed Sema3A-induced colocalization of PlexA4 and TrkA in the growth cones and axons (Fig.…”

Section: Sema3a-induced Clathrin-dependent Colocalization Of Plexa4 Amentioning

confidence: 58%

“…In Xenopus commissural interneurons, it has been suggested that Sema3A increases the number of Ca v 2.3 channels in the growth cone plasma membrane rather than modulating their gating properties (Nishiyama et al, 2011). Further studies will be required to determine whether CRMP1 regulates membrane trafficking of Na v 1.7 and/or it modulates the channel properties of Na v 1.7.…”

Section: Discussionmentioning

confidence: 99%

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A functional coupling between CRMP1 and Nav1.7 for retrograde propagation of Semaphorin3A signaling

Yamane

Yamashita

Hida

et al. 2017

Journal of Cell Science

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Semaphorin3A (Sema3A) is a secreted type of axon guidance molecules that regulates axon wiring through neuropilin-1 (NRP1) and PlexinAs (PlexAs) receptor complex. Sema3A regulates the dendritic branching through a tetrodotoxin (TTX)-sensitive retrograde axonal transport of PlexAs and Tropomyosin-related kinase A (TrkA) complex. We here demonstrate that Nav1.7, a TTX-sensitive Na+ channel, by coupling with collapsin response mediator protein 1 (CRMP1), mediates the Sema3A-induced retrograde transport. In mouse dorsal root ganglion (DRG) neurons, Sema3A increased co-localization of PlexA4 and TrkA in the growth cones and axons. TTX treatment and RNAi knockdown of Nav1.7, sustained Sema3A-induced co-localized signals of PlexA4 and TrkA in growth cones, and suppressed the subsequent localization of PlexA4 and TrkA in distal axons. A similar localization phenotype was observed in crmp1−/− DRG neurons. Sema3A induced co-localization of CRMP1 and Nav1.7 in the growth cones. The half maximal voltage was increased in crmp1−/− neurons when compared to wild-type. In HEK293 cells, introduction of CRMP1 lowered the threshold of the coexpressed Nav1.7. These results suggest that Nav1.7 mediates through coupling with CRMP1 the axonal retrograde signaling of Sema3A.

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Section: Sema3a-induced Clathrin-dependent Colocalization Of Plexa4 Amentioning

confidence: 58%

Section: Discussionmentioning

confidence: 99%

A functional coupling between CRMP1 and Nav1.7 for retrograde propagation of Semaphorin3A signaling

Yamane

Yamashita

Hida

et al. 2017

Journal of Cell Science

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“…For example, the dendrites of Xenopus spinal cord interneurons emerge from the proximal axon (Nishiyama et al, 2011), whereas for cultured mouse hippocampal neurons, dendrite polarization probably occurs secondary to the inhibition of axon initiation (Shelly et al, 2011). Polarization of the axon and dendrites of the retinal ganglion cell (RGC), however, appears to occur independently.…”

Section: Introductionmentioning

confidence: 99%

Neuropilin-1 biases dendrite polarization in the retina

et al. 2013

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SUMMARYThe majority of neurons in the nervous system exhibit a polarized morphology, with multiple short dendrites and a single long axon. It is clear that multiple factors govern polarization in developing neurons, and the biased accumulation of intrinsic determinants to one side of the cell, coupled with responses to asymmetrically localized extrinsic factors, appears to be crucial. A number of intrinsic factors have been identified, but surprisingly little is known about the identity of the extrinsic signals. Here, we show in vivo that neuropilin-1 (Nrp1) and its co-receptor plexinA1 (Plxna1) are necessary to bias the extension of the dendrites of retinal ganglion cells to the apical side of the cell, and ectopically expressed class III semaphorins (Sema3s) disrupt this process. Importantly, the requirement for Nrp1 and Plxna1 in dendrite polarization occurs at a developmental time point after the cells have already extended their basally directed axon. Thus, we propose a novel mechanism whereby an extrinsic factor, probably a Sema3, acts through Nrp1 and Plxna1 to promote the asymmetric outgrowth of dendrites independently of axon polarization.

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“…53,54 The coupling mechanism upon Sema3A stimulation between Ca 2C channels and Na C channels is unknown. Although several L-type Ca 2C channel blockers suppress Sema3A-induced axonal transport, 54,55 the voltage-dependent Ca 2C channels that mediate Sema3A response may include R-type Ca 2C channels, as demonstrated in Xenopus spinal neurons, 64 and in embryonic day 15 (E15) mouse DRG. 65 Indeed, despite minor effect, nimodipine suppresses R-type Ca 2C channels, and R-type Ca 2C channels contribute to fast synaptic excitation and action potentials in guinea pig myenteric neurons.…”

Section: Background: Dendritic Development Regulated By Semaphorinsmentioning

confidence: 99%

Regulation of dendritic development by semaphorin 3A through novel intracellular remote signaling

Goshima

Yamashita

Nakamura

et al. 2016

Cell Adhesion & Migration

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Numerous cell adhesion molecules, extracellular matrix proteins and axon guidance molecules participate in neuronal network formation through local effects at axo-dendritic, axo-axonic or dendro-dendritic contact sites. In contrast, neurotrophins and their receptors play crucial roles in neural wiring by sending retrograde signals to remote cell bodies. Semaphorin 3A (Sema3A), a prototype of secreted type 3 semaphorins, is implicated in axon repulsion, dendritic branching and synapse formation via binding protein neuropilin-1 (NRP1) and the signal transducing protein PlexinAs (PlexAs) complex. This review focuses on Sema3A retrograde signaling that regulates dendritic localization of AMPA-type glutamate receptor GluA2 and dendritic patterning. This signaling is elicited by activation of NRP1 in growth cones and is propagated to cell bodies by dynein-dependent retrograde axonal transport of PlexAs. It also requires interaction between PlexAs and a high-affinity receptor for nerve growth factor, toropomyosin receptor kinase A. We propose a control mechanism by which retrograde Sema3A signaling regulates the glutamate receptor localization through trafficking of cis-interacting PlexAs with GluA2 along dendrites; this remote signaling may be an alternative mechanism to local adhesive contacts for neural network formation.

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Semaphorin 3A induces CaV2.3 channel-dependent conversion of axons to dendrites

Cited by 46 publications

References 50 publications

A functional coupling between CRMP1 and Nav1.7 for retrograde propagation of Semaphorin3A signaling

A functional coupling between CRMP1 and Nav1.7 for retrograde propagation of Semaphorin3A signaling

Neuropilin-1 biases dendrite polarization in the retina

Regulation of dendritic development by semaphorin 3A through novel intracellular remote signaling

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