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Published 11 April 2005. doi:10.1083/jcb.200409140
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 169, Number 1, 127-138
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Article

A Rho family GTPase controls actin dynamics and tip growth via two counteracting downstream pathways in pollen tubes



Ying Gu1,2, Ying Fu1,2, Peter Dowd3, Shundai Li1,2, Vanessa Vernoud1,2, Simon Gilroy4, and Zhenbiao Yang1,2

1 Center for Plant Cell Biology, Institute for Integrative Genome Biology
2 Department of Botany and Plant Sciences, University of California, Riverside, Riverside, CA 92521
3 Department of Biochemistry and Molecular Biology, Pennsylvania State University, State College, PA 16802
4 Department of Biology, Pennsylvania State University, State College, PA 16802

Correspondence to Z. Yang: zhenbiao.yang{at}ucr.edu

Tip growth in neuronal cells, plant cells, and fungal hyphae is known to require tip-localized Rho GTPase, calcium, and filamentous actin (F-actin), but how they interact with each other is unclear. The pollen tube is an exciting model to study spatiotemporal regulation of tip growth and F-actin dynamics. An Arabidopsis thaliana Rho family GTPase, ROP1, controls pollen tube growth by regulating apical F-actin dynamics. This paper shows that ROP1 activates two counteracting pathways involving the direct targets of tip-localized ROP1: RIC3 and RIC4. RIC4 promotes F-actin assembly, whereas RIC3 activates Ca2+ signaling that leads to F-actin disassembly. Overproduction or depletion of either RIC4 or RIC3 causes tip growth defects that are rescued by overproduction or depletion of RIC3 or RIC4, respectively. Thus, ROP1 controls actin dynamics and tip growth through a check and balance between the two pathways. The dual and antagonistic roles of this GTPase may provide a unifying mechanism by which Rho modulates various processes dependent on actin dynamics in eukaryotic cells.

Abbreviations used in this paper: CRIB, Cdc42/Rac interactive binding; FRET, fluorescence resonance energy transfer; LatB, latrunculin B; LOF, loss-of-function; OX, overexpression; PM, plasma membrane; WT, wild-type.


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