ArticleThe Journal of cell biology2000
Semaphorin3A enhances endocytosis at sites of receptor-F-actin colocalization during growth cone collapse.
Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 210 citations in OpenAlex.
- Trio and CRMP2 regulate axon branching and Semaphorin3A signaling.Communications biology · 2025Article
- SEMA3B switches axon-axon to axon-glia interactions required for unmyelinated axon envelopment and integrity.Nature communications · 2025Article
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- Metastatic organotropism in small cell lung cancer.bioRxiv : the preprint server for biology · 2025Article
- Invasion of glioma cells through confined space requires membrane tension regulation and mechano-electrical coupling via Plexin-B2.Nature communications · 2025Article
- TRIM9 Controls Growth Cone Responses to Netrin Through DCC and UNC5C.Journal of neurochemistry · 2025Article
- Semmaphorin 3 A causes immune suppression by inducing cytoskeletal paralysis in tumour-specific CD8Nature communications · 2024Article
- Differential modulation of cell morphology, migration, and Neuropilin-1 expression in cancer and non-cancer cell lines by substrate stiffness.Frontiers in cell and developmental biology · 2024Article
- Syntaxin-1 is necessary for UNC5A-C/Netrin-1-dependent macropinocytosis and chemorepulsion.Frontiers in molecular neuroscience · 2023Article
- Neuropilin 1 and its inhibitory ligand mini-tryptophanyl-tRNA synthetase inversely regulate VE-cadherin turnover and vascular permeability.Nature communications · 2022Article
- Rabphilin3A reduces integrin-dependent growth cone signaling to restrict axon regeneration after trauma.Experimental neurology · 2022Article
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- Identification and Functional Characterization of a Novel Variant in theInternational journal of endocrinology · 2022Article
- A CRMP4-dependent retrograde axon-to-soma death signal in amyotrophic lateral sclerosis.The EMBO journal · 2021Article
- SH3BP4 promotes neuropilin-1 and α5-integrin endocytosis and is inhibited by Akt.Developmental cell · 2021Article
- Long-distance regressive signaling in neural development and disease.Wiley interdisciplinary reviews. Developmental biology · 2021Review
- SLIT2/ROBO1-signaling inhibits macropinocytosis by opposing cortical cytoskeletal remodeling.Nature communications · 2020Article
- Deficiency in the secreted protein Semaphorin3d causes abnormal parathyroid development in mice.The Journal of biological chemistry · 2019Article
- A Subtle Network Mediating Axon Guidance: Intrinsic Dynamic Structure of Growth Cone, Attractive and Repulsive Molecular Cues, and the Intermediate Role of Signaling Pathways.Neural plasticity · 2019Review
- Functional Genome-wide Screen Identifies Pathways Restricting Central Nervous System Axonal Regeneration.Cell reports · 2018Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Axonal growth cone collapse is accompanied by a reduction in filopodial F-actin. We demonstrate here that semaphorin 3A (Sema3A) induces a coordinated rearrangement of Sema3A receptors and F-actin during growth cone collapse. Differential interference contrast microscopy reveals that some sites of Sema3A-induced F-actin reorganization correlate with discrete vacuoles, structures involved in endocytosis. Endocytosis of FITC-dextran by the growth cone is enhanced during Sema3A treatment, and sites of dextran accumulation colocalize with actin-rich vacuoles and ridges of membrane. Furthermore, the Sema3A receptor proteins, neuropilin-1 and plexin, and the Sema3A signaling molecule, rac1, also reorganize to vacuoles and membrane ridges after Sema3A treatment. These data support a model whereby Sema3A stimulates endocytosis by focal and coordinated rearrangement of receptor and cytoskeletal elements. Dextran accumulation is also increased in retinal ganglion cell (RGC) growth cones, in response to ephrin A5, and in RGC and DRG growth cones, in response to myelin and phorbol-ester. Therefore, enhanced endocytosis may be a general principle of physiologic growth cone collapse. We suggest that growth cone collapse is mediated by both actin filament rearrangements and alterations in membrane dynamics.
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