Semaphorin3A enhances endocytosis at sites of receptor-F-actin colocalization during growth cone collapse

Alyson E. Fournier, Fumio Nakamura, Susumu Kawamoto, Yoshio Goshima, Robert G. Kalb, Stephen M. Strittmatter*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

170 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)411-421
Number of pages11
JournalJournal of Cell Biology
Issue number2
StatePublished - Apr 17 2000


  • Axon guidance
  • Axon repulsion
  • Dextran uptake
  • Ephrins
  • Membrane dynamics

ASJC Scopus subject areas

  • Cell Biology

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