Growth cone neuropilin-1 mediates collapsin-1/sema III facilitation of antero- and retrograde axoplasmic transport

Goshima, Yoshio; Hori, Hideaki; Sasaki, Yukio; Yang, Tao; Kagoshima-Maezono, Masako; Li, Chanxia; Takenaka, Toshifumi; Nakamura, Fumio; Takahashi, Takuya; Strittmatter, Stephen M.; Misu, Yoshimi; Kawakami, Tadashi

doi:10.1002/(sici)1097-4695(19990615)39:4<579::aid-neu11>3.0.co;2-9

Cited by 47 publications

(42 citation statements)

References 29 publications

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“…Using time-lapse video microscopy, we previously demonstrated that Sema3A facilitates organelle transport along axon of dorsal root ganglion (DRG) neurons, pseudounipolar neurons that contain an axon splitting into two branches 21 . Sema3A transiently facilitates the percentage of moving particles, and these particles monitored by time-lapse video microscopy are composed mainly of mitochondria and non-mitochondrial particles 10,21 . The transported particles observed generally have maximal diameters of 40.2 mm, and the velocity of these moving particles ranges from 0.6 to 4.5 mm s À 1 in both antero-and retrograde transport.…”

Section: Resultsmentioning

confidence: 99%

“…UNC-6/netrin also mediates adhesive interactions to promote synaptogenesis 6 . Semaphorin 3A (Sema3A) is a secreted protein identified as a factor that collapses and paralyses the neuronal growth cone by acting on a growth cone receptor complex of neuropilin1 (NRP1) and plexinAs (PlexAs) [7][8][9][10] . Sema3A has multiple functions in the regulation of both axonal and dendritic development.…”

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confidence: 99%

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Plexin-A4-dependent retrograde semaphorin 3A signalling regulates the dendritic localization of GluA2-containing AMPA receptors

et al. 2014

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The dendritic targeting of neurotransmitter receptors is vital for dendritic development and function. However, how such localization is established remains unclear. Here we show that semaphorin 3A (Sema3A) signalling at the axonal growth cone is propagated towards the cell body by retrograde axonal transport and drives AMPA receptor GluA2 to the distal dendrites, which regulates dendritic development. Sema3A enhances glutamate receptor interacting protein 1-dependent localization of GluA2 in dendrites, which is blocked by knockdown of cytoplasmic dynein heavy chain. PlexinA (PlexA), a receptor component for Sema3A, interacts with GluA2 at the immunoglobulin-like Plexin-transcription-factor domain (PlexA-IPT) in somatodendritic regions. Overexpression of PlexA-IPT suppresses dendritic localization of GluA2 and induces aproximal bifurcation phenotype in the apical dendrites of CA1 hippocampal neurons. Thus, we propose a control mechanism by which retrograde Sema3A signalling regulates the glutamate receptor localization through trafficking of cis-interacting PlexA with GluA2 along dendrites.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

Plexin-A4-dependent retrograde semaphorin 3A signalling regulates the dendritic localization of GluA2-containing AMPA receptors

et al. 2014

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“…We used immunofluorescence staining because it enabled us to focus exclusively on growth cones-the cellular compartment where guidance receptors are operating. Thus, our analysis excluded Nrp1 molecules that are highly abundant on the surface of axons 42 , but do not mediate Sema3A signalling 43 . Nrp1 molecules, expressed by Schwann cells and DRG-associated fibroblasts in the culture 44 , were avoided as well.…”

Section: Resultsmentioning

confidence: 99%

ADAM metalloproteases promote a developmental switch in responsiveness to the axonal repellant Sema3A

et al. 2014

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During embryonic development, axons can gain and lose sensitivity to guidance cues, and this flexibility is essential for the correct wiring of the nervous system. Yet, the underlying molecular mechanisms are largely unknown. Here we show that receptor cleavage by ADAM (A Disintegrin And Metalloprotease) metalloproteases promotes murine sensory axons loss of responsiveness to the chemorepellant Sema3A. Genetic ablation of ADAM10 and ADAM17 disrupts the developmental downregulation of Neuropilin-1 (Nrp1), the receptor for Sema3A, in sensory axons. Moreover, this is correlated with gain of repulsive response to Sema3A. Overexpression of Nrp1 in neurons reverses axonal desensitization to Sema3A, but this is hampered in a mutant Nrp1 with high susceptibility to cleavage. Lastly, we detect guidance errors of proprioceptive axons in ADAM knockouts that are consistent with enhanced response to Sema3A. Our results provide the first evidence for involvement of ADAMs in regulating developmental switch in responsiveness to axonal guidance cues.

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“…Other biological actions of Sema3A include regulation of dendritic patterning, synapse maturation, neural cell polarity and axonal transport (Goshima et al, 1999(Goshima et al, , 1997Li et al, 2004;Nakamura et al, 2009;Sasaki et al, 2002;Tran et al, 2009;Yamashita et al, 2007Yamashita et al, , 2014. Sema3A-induced axonal transport could play an essential role in mediating some of the biological activities of Sema3A (Goshima et al, 2016;Yamashita et al, 2014Yamashita et al, , 2016c.…”

Section: Introductionmentioning

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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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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Growth cone neuropilin-1 mediates collapsin-1/sema III facilitation of antero- and retrograde axoplasmic transport

Cited by 47 publications

References 29 publications

Plexin-A4-dependent retrograde semaphorin 3A signalling regulates the dendritic localization of GluA2-containing AMPA receptors

Plexin-A4-dependent retrograde semaphorin 3A signalling regulates the dendritic localization of GluA2-containing AMPA receptors

ADAM metalloproteases promote a developmental switch in responsiveness to the axonal repellant Sema3A

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

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