JCB logo
Quantitative Colocalization Analysis Software
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 30 September 2002. doi:10.1083/jcb.200204140
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 401K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gallo, G.
Right arrow Articles by Letourneau, P. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gallo, G.
Right arrow Articles by Letourneau, P. C.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

© The Rockefeller University Press, 0021-9525/2002/9/1219 $5.00
The Journal of Cell Biology, Volume 158, Number 7, September 30, 2002 1219-1228

Article

Actin turnover is required to prevent axon retraction driven by endogenous actomyosin contractility



Gianluca Gallo1, Hal F. Yee, Jr.2 and Paul C. Letourneau1

1 Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455
2 Department of Medicine and Physiology, University of California Los Angeles, Los Angeles, CA 90095

Address correspondence to Gianluca Gallo at his present address, Dept. of Neurobiology and Anatomy, Drexel Univ. College of Medicine, 2900 Queen Ln., Philadelphia, PA 19129. Tel.: (215) 991-8288. Fax: (215) 843-9082. E-mail: Neurite{at}aol.com

Growth cone motility and guidance depend on the dynamic reorganization of filamentous actin (F-actin). In the growth cone, F-actin undergoes turnover, which is the exchange of actin subunits from existing filaments. However, the function of F-actin turnover is not clear. We used jasplakinolide (jasp), a cell-permeable macrocyclic peptide that inhibits F-actin turnover, to study the role of F-actin turnover in axon extension. Treatment with jasp caused axon retraction, demonstrating that axon extension requires F-actin turnover. The retraction of axons in response to the inhibition of F-actin turnover was dependent on myosin activity and regulated by RhoA and myosin light chain kinase. Significantly, the endogenous myosin-based contractility was sufficient to cause axon retraction, because jasp did not alter myosin activity. Based on these observations, we asked whether guidance cues that cause axon retraction (ephrin-A2) inhibit F-actin turnover. Axon retraction in response to ephrin-A2 correlated with decreased F-actin turnover and required RhoA activity. These observations demonstrate that axon extension depends on an interaction between endogenous myosin-driven contractility and F-actin turnover, and that guidance cues that cause axon retraction inhibit F-actin turnover.

Key Words: jasplakinolide; RhoA; ephrin; cytoskeleton; myosin


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents