Document Detail


Rac is required for growth cone function but not neurite assembly.
MedLine Citation:
PMID:  9092945     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recent work has suggested that rac1 and other members of the rho family of small GTP-binding proteins play an important role in the formation of neural processes. We have explored the mechanism of this effect by comparing the spontaneous, growth cone-mediated growth and experimental tension-induced growth of axons in normal PC12 cells and in mutant cells expressing a dominant negative form of rac. PC12 that have been primed by exposure to NGF, but not naive PC12 cells, initiate a microtubule-rich process de novo in response to tension applied to cell body. As in chick sensory neurons, neurite elongation rate is proportional to applied tension above a threshold. Addition of cyclic AMP, which has been shown to rapidly augment NGF-induced neurite outgrowth in PC12, causes a rapid increase in the rate of neurite elongation at a given tension level. Expression of a dominant negative form of rac1 inhibits spontaneous, growth cone-mediated neurite elongation in response to NGF, but does not substantially affect tension-induced neurite elongation. That is, rac-deficient cells show a normal linear relationship between applied tension and elongation rate and the elongations contain a normal density of axial microtubules by immunofluorescent assay. Thus, rac1 is apparently required for the mechanisms that normally generate tension in an elongating neurite, but if this tension is provided from an outside source, then axonal elongation can proceed normally in rac1-deficient cells. We conclude that rac1 is required for the adhesive and motile function of growth cones rather than the assembly of neurites per se.
Authors:
P Lamoureux; Z F Altun-Gultekin; C Lin; J A Wagner; S R Heidemann
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of cell science     Volume:  110 ( Pt 5)     ISSN:  0021-9533     ISO Abbreviation:  J. Cell. Sci.     Publication Date:  1997 Mar 
Date Detail:
Created Date:  1997-06-06     Completed Date:  1997-06-06     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0052457     Medline TA:  J Cell Sci     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  635-41     Citation Subset:  IM    
Affiliation:
Department of Physiology, Michigan State University, East Lansing 48824, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Axons / physiology*
Cell Division / genetics
GTP-Binding Proteins / genetics,  physiology*
Genes, Dominant
Microscopy, Fluorescence
Mutation
Nerve Growth Factors / pharmacology
Neurites / physiology*
PC12 Cells
Rats
rac GTP-Binding Proteins
Grant Support
ID/Acronym/Agency:
EY06454/EY/NEI NIH HHS; GM36894/GM/NIGMS NIH HHS; NS31728/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Nerve Growth Factors; EC 3.6.1.-/GTP-Binding Proteins; EC 3.6.5.2/rac GTP-Binding Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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