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Published on August 17, 2007; 10.1104/pp.107.106021

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Received July 23, 2007
Accepted August 9, 2007

Dual Regulation Role of GH3.5 in Salicylic Acid and Auxin Signaling during Arabidopsis-Pseudomonas syringae Interaction

Zhongqin Zhang , Qun Li , Zhimiao Li , Paul E. Staswick , Muyang Wang , Ying Zhu , and Zuhua He *

National Key Laboratory of Plant Molecular Genetics, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China; and Institute of Vegetables, Zhejiang Academy of Agricultural Sciences, Hangzhou, China: and Department of Agronomy and Horticulture, University of Nebraska, Lincoln, Nebraska, United States of America

* Corresponding author; email: zhhe{at}sibs.ac.cn.

Salicylic acid (SA) plays a central role in plant disease resistance, and emerging evidence indicates that auxin, an essential plant hormone in regulating plant growth and development, is involved in plant disease susceptibility. GH3.5, a member of the GH3 family of early auxin-responsive genes in Arabidopsis, encodes a protein possessing an in vitro adenylation activity on both indole-3-acetic acid (IAA) and SA. Here we show that GH3.5 acts as a bifunctional modulator in both SA and auxin signaling during pathogen infection. Overexpression of the GH3.5 gene in an activation-tagged mutant gh3.5-1D led to elevated accumulation of SA and increased expression of PR-1 in local and systemic tissues in response to avirulent pathogens. In contrast, two T-DNA insertional mutations of GH3.5 partially compromised the systemic acquired resistance (SAR) associated with diminished PR-1 expression in systemic tissues. The gh3.5-1D mutant also accumulated high levels of free IAA after pathogen infection and had impaired different R gene-mediated resistance, which was also observed in the GH3.6 activation-tagged mutant dfl1-D that impacted the auxin pathway, indicating an important role of GH3.5/GH3.6 in disease susceptibility. Furthermore, microarray analysis showed that the SA and auxin pathways were simultaneously augmented in gh3.5-1D after infection with an avirulent pathogen. The SA pathway was amplified by GH3.5 through inducing SA-responsive genes, basal defense components; while the auxin pathway was derepressed through up-regulating IAA biosynthesis and down-regulating auxin repressor genes. Taken together, our data reveals novel regulatory functions of GH3.5 in the plant-pathogen interaction.




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