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Molecular and Cellular Biology, October 2000, p. 7378-7387, Vol. 20, No. 19
Laboratory of Molecular Neurobiology,
Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto
606-8502, Japan
Received 11 May 2000/Returned for modification 14 June
2000/Accepted 3 July 2000
The Rho family of small GTPases has been implicated in cytoskeletal
reorganization and subsequent morphological changes in various
cell types. Among them, Rac and Cdc42 have been shown to be involved in
neurite outgrowth in neuronal cells. In this study, we examined the
role of RhoG, another member of Rho family GTPases, in nerve growth
factor (NGF)-induced neurite outgrowth in PC12 cells. Expression of
wild-type RhoG in PC12 cells induced neurite outgrowth in the absence
of NGF, and the morphology of wild-type RhoG-expressing cells was
similar to that of NGF-differentiated cells. Constitutively active
RhoG-transfected cells extended short neurites but developed large
lamellipodial or filopodial structures at the tips of neurites.
RhoG-induced neurite outgrowth was inhibited by coexpression with
dominant-negative Rac1 or Cdc42. In addition, expression of
constitutively active RhoG elevated endogenous Rac1 and Cdc42
activities. We also found that the NGF-induced neurite outgrowth was
enhanced by expression of wild-type RhoG whereas expression of
dominant-negative RhoG suppressed the neurite outgrowth. Furthermore,
constitutively active Ras-induced neurite outgrowth was also suppressed
by dominant-negative RhoG. Taken together, these results suggest that
RhoG is a key regulator in NGF-induced neurite outgrowth, acting
downstream of Ras and upstream of Rac1 and Cdc42 in PC12 cells.
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Small GTPase RhoG Is a Key Regulator for
Neurite Outgrowth in PC12 Cells
*
Corresponding author. Mailing address: Laboratory of
Molecular Neurobiology, Graduate School of Biostudies, Kyoto
University, Sakyo-ku, Kyoto 606-8502, Japan. Phone: 81-75-753-4547. Fax: 81-75-753-7688. E-mail:
mnegishi{at}pharm.kyoto-u.ac.jp.
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