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© The Rockefeller University Press, 0021-9525/1998//175 $5.00
The Journal of Cell Biology, Volume 141, Number 1, , 1998 175-185

Regular Articles

Rho Guanosine Triphosphatase Mediates the Selective Stabilization of Microtubules Induced by Lysophosphatidic Acid



Tiffani A. Cook*,{ddagger}, Takayuki Nagasaki*, and Gregg G. Gundersen*,||

* Department of Anatomy and Cell Biology, {ddagger} Integrated Program in Cellular, Molecular, and Biophysical Studies, and || Department of Pathology, Columbia University, New York

The asymmetric distribution of stable, posttranslationally modified microtubules (MTs) contributes to the polarization of many cell types, yet the factors controlling the formation of these MTs are not known. We have found that lysophosphatidic acid (LPA) is a major serum factor responsible for rapidly generating stable, detyrosinated (Glu) MTs in serum-starved 3T3 cells. Using C3 toxin and val14 rho we showed that rho was both necessary and sufficient for the induction of Glu MTs by LPA and serum. Unlike previously described factors that induce MT stability, rho induced the stabilization of only a subset of the MTs and, in wound-edge cells, these stable MTs were appropriately oriented toward the leading edge of the cell. LPA had little effect on individual parameters of MT dynamics, but did induce long states of pause in a subset of MTs near the edge of the cell. Rho stimulation of MT stability was independent of actin stress fiber formation. These results identify rho as a novel regulator of the MT cytoskeleton that selectively stabilizes MTs during cell polarization by acting as a switch between dynamic and stable states of MTs rather than as a modulator of MT assembly and disassembly.

Abbreviations used in this paper: Glu, detyrosinated; LPA, lysophosphatidic acid; MT, microtubule; PLB, phospholipase B; SFM, serum-free medium; Tyr, tyrosinated.

T.A. Cook was supported by an National Institutes of Health training grant through the Integrated Program in Cellular, Molecular, and Biophysical Studies. T. Nagasaki was supported by a Damon Runyon-Walter Winchell Postdoctoral Fellowship. This research was supported by a grant from the American Cancer Society to G.G. Gundersen.

Address all correspondence to Gregg Gundersen, Department of Anatomy and Cell Biology, Columbia University, 630 West 168th Street, New York, NY 10032. Tel.: (212) 305-1899. Fax: (212) 305-3970. E-mail: ggg1{at}columbia.edu


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