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J. Biol. Chem., Vol. 282, Issue 13, 10036-10046, March 30, 2007

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GH3-mediated Auxin Homeostasis Links Growth Regulation with Stress Adaptation Response in Arabidopsis^*

Jung-Eun Park, Ju-Young Park, Youn-Sung Kim, Paul E. Staswick^¶, Jin Jeon^||, Ju Yun, Sun-Young Kim, Jungmook Kim^||, Yong-Hwan Lee, and Chung-Mo Park¹

From the Molecular Signaling Laboratory, Department of Chemistry, Seoul National University, Seoul 151-742, Korea, the School of Agricultural Biotechnology and Center for Agricultural Biomaterials, Seoul National University, Seoul 151-742, Korea, the ^¶Department of Agronomy and Horticulture, University of Nebraska, Lincoln, Nebraska 68583, and the ^||Department of Plant Biotechnology, Agricultural Plant Stress Research Center and Biotechnology Research Institute, Chonnam National University, Gwangju 500-757, Korea

Plants constantly monitor environmental fluctuations to optimize their growth and metabolism. One example is adaptive growth occurring in response to biotic and abiotic stresses. Here, we demonstrate that GH3-mediated auxin homeostasis is an essential constituent of the complex network of auxin actions that regulates stress adaptation responses in Arabidopsis. Endogenous auxin pool is regulated, at least in part, through negative feedback by a group of auxin-inducible GH3 genes encoding auxin-conjugating enzymes. An Arabidopsis mutant, wes1-D, in which a GH3 gene WES1 is activated by nearby insertion of the ³⁵S enhancer, exhibited auxin-deficient traits, including reduced growth and altered leaf shape. Interestingly, WES1 is also induced by various stress conditions as well as by salicylic acid and abscisic acid. Accordingly, wes1-D was resistant to both biotic and abiotic stresses, and stress-responsive genes, such as pathogenesis-related genes and CBF genes, were upregulated in this mutant. In contrast, a T-DNA insertional mutant showed reduced stress resistance. We therefore propose that GH3-mediated growth suppression directs reallocation of metabolic resources to resistance establishment and represents the fitness costs of induced resistance.

Received for publication, November 13, 2006 , and in revised form, January 8, 2007.

^* This work was supported by the BK 21, Biogreen 21 (20050301034456) and National Research Laboratory programs, a grant from the Plant Signaling Network Research Center, Korea Science and Engineering Foundation Grant R02-2003-000-10001-0, Korea Research Foundation Grant 2005-070-C00129, and Plant Diversity Research Center of 21st Century Frontier Research Program Grant PF0330404-02 (to J. K.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1-S5.

¹ To whom correspondence should be addressed. Tel.: 82-2-880-6640; Fax: 82-2-889-1568; E-mail: cmpark{at}snu.ac.kr.

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