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Plant Physiology 134 (1): 129-136

Copyright © 2004 by the American Society of Plant Physiologists.


Phosphatidic Acid Induces Leaf Cell Death in Arabidopsis by Activating the Rho-Related Small G Protein GTPase-Mediated Pathway of Reactive Oxygen Species Generation1

Jumok Park, Ying Gu, Yuree Lee, Zhenbiao Yang, and Youngsook Lee*

Division of Molecular Life Science, Pohang University of Science and Technology, Pohang, 790-784, Korea (J.P., Yu.L., Yo.L.); and Center for Plant Cell Biology and Department of Botany and Plant Sciences, University of California, Riverside, California 92521-0124 (Y.G., Z.Y.)

Abstract: Phosphatidic acid (PA) level increases during various stress conditions. However, the physiological roles of this lipid in stress response remain largely unknown. In this study, we report that PA induced leaf cell death and elevated the levels of reactive oxygen species (ROS) in the whole leaf and single cells. To further elucidate the mechanism of PA-induced cell death, we then examined whether Rho-related small G protein (ROP) 2, which enhanced ROS production in an in vitro assay, is involved in PA-induced ROS production and cell death. In response to PA, transgenic leaves of Arabidopsis expressing a constitutively active rop2 mutant exhibited earlier cell death and higher levels of ROS than wild type (WT), whereas those expressing a dominant-negative rop2 mutant exhibited later cell death and lower ROS. However, in the absence of exogenous PA, no spontaneous cell death or elevated ROS was observed in constitutively active rop2 plants, suggesting that the activation of ROP GTPase alone is insufficient to activate the ROP-mediated ROS generation pathway. These results suggest that PA modulates an additional factor required for the active ROP-mediated ROS generation pathway. Therefore, PA may be an important regulator of ROP-regulated ROS generation and the cell death process during various stress and defense responses of plants.

Article, publication date, and citation information can be found at

1 This work was supported by the Korea Research Foundation (grant no. KRF-2001-015-DS0052) and by the Korea Science and Engineering Foundation (grant no. 2000-6-203-01-2) awarded to Y.L. and Z.Y.

* Corresponding author; e-mail ylee{at}; fax 82-54-279-2199.

Received for publication August 6, 2003. Revision received September 14, 2003. Accepted for publication September 14, 2003.

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