Send to

Choose Destination
See comment in PubMed Commons below
J Neurobiol. 2003 Feb 5;54(2):358-69.

Independent roles of Rho-GTPases in growth cone and axonal behavior.

Author information

  • 1Max-Planck Unit for Structural Molecular Biology, c/o Desy, Hamburg, Germany.


Many external signals influence growth cone motility, pathfinding, and the formation of synapses that lead to the final map formation of the retinotectal system. Chick temporal retinal ganglion cell axons (RGCs) collapse and retract after encountering posterior tectal cells in vitro. During this process lateral extensions appear along the RGC axonal shaft. Lateral extensions appear as nascent interstitial axonal branches and also as defasciculating growth cones that are trailing along the pioneer axon. RGC branching controlled by repellent tectal cues has recently been shown to be the critical event in retinotectal map development. The intracellular mechanism underlying this phenomenon, however, is not understood. Inhibiting RhoA with either C3 toxin or inhibiting p160Rock kinase, an effector of RhoA, with Y27632 inhibited collapse, retraction, and the number of axons that showed lateral extensions. Lateral extension length increased significantly. Inhibiting Rac1A and cdc42 with cell permeable peptide inhibitors did not inhibit collapse of growth cones, but did inhibit axon retraction. In addition, the number of axons that showed lateral extensions and lateral extension length were significantly reduced. A dynamic cytoskeleton is necessary to react to incoming guidance information. This study addresses the problems of how growth cone motility and branching or defasciculation are affected by Rho-GTPases as extracellular signals are transmitted to the cytoskeleton.

Copyright 2002 Wiley Periodicals, Inc.

[PubMed - indexed for MEDLINE]
Free full text

LinkOut - more resources

Full Text Sources

Other Literature Sources

PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Write to the Help Desk