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

Treinys, Rimantas; Kaselis, Andrius; Jover, Emmanuel; Bagnard, Dominique; Šatkauskas, Saulius

doi:10.1371/journal.pone.0102357

Cited by 10 publications

(8 citation statements)

References 66 publications

(81 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: 71%

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: 71%

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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“…More intriguingly, recent evidence suggests that Sema3A increases calcium influx through R-type calcium channels in cultured mouse sensory neurons. 48 We speculate that repulsive axon guidance molecules might coordinately regulate wiring of the nervous and vascular networks through shared effectors and mechanisms ( Figure 6C), and this is an interesting direction of future studies.…”

Section: /Calmodulin Binding Inhibits Tie2 Signaling 1415mentioning

confidence: 92%

Calmodulin Mediates Ca ²⁺ -Dependent Inhibition of Tie2 Signaling and Acts as a Developmental Brake During Embryonic Angiogenesis

Yang

Ohk

Lee

et al. 2016

ATVB

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Objective-Angiogenesis, the process of building complex vascular structures, begins with sprout formation on preexisting blood vessels, followed by extension of the vessels through proliferation and migration of endothelial cells. Based on the potential therapeutic benefits of preventing angiogenesis in pathological conditions, many studies have focused on the mechanisms of its initiation as well as control. However, how the extension of vessels is terminated remains obscure. Thus, we investigated the negative regulation mechanism. Approach and Results-We report that increased intracellular calcium can induce dephosphorylation of the endothelial receptor tyrosine kinase Tie2. The calcium-mediated dephosphorylation was found to be dependent on Tie2-calmodulin interaction. The Tyr1113 residue in the C-terminal end loop of the Tie2 kinase domain was mapped and found to be required for this interaction. Moreover, mutation of this residue into Phe impaired both the Tie2-calmodulin interaction and calcium-mediated Tie2 dephosphorylation. Furthermore, expressing a mutant Tie2 incapable of binding to calmodulin or inhibiting calmodulin function in vivo causes unchecked growth of the vasculature in Xenopus. Specifically, knockdown of Tie2 in Xenopus embryo retarded the sprouting and extension of intersomitic veins. Although human Tie2 expression in the Tie2-deficient animals almost completely rescued the retardation, the Tie2(Y1113F) mutant caused overgrowth of intersomitic veins with strikingly complex and excessive branching patterns. Conclusions-We propose that the calcium/calmodulin-dependent negative regulation of Tie2 can be used as an inhibitory signal for vessel growth and branching to build proper vessel architecture during embryonic development.

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“…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. 66 Thus it is possible that Sema3A activates the R-type Ca 2C channels in the growth cones, thereby leading to opening the Na C channels in the growth cones and/2r axons.…”

Section: Background: Dendritic Development Regulated By Semaphorinsmentioning

confidence: 98%

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

Cited by 10 publications

References 66 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

Calmodulin Mediates Ca ²⁺ -Dependent Inhibition of Tie2 Signaling and Acts as a Developmental Brake During Embryonic Angiogenesis

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

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

Cited by 10 publications

References 66 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

Calmodulin Mediates Ca 2+ -Dependent Inhibition of Tie2 Signaling and Acts as a Developmental Brake During Embryonic Angiogenesis

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

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Calmodulin Mediates Ca ²⁺ -Dependent Inhibition of Tie2 Signaling and Acts as a Developmental Brake During Embryonic Angiogenesis