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

文献类型： 外文期刊

作者： Zhang, Zhongqin 1 ; Li, Qun 2 ; Li, Zhimiao 2 ; Staswick, Paul E. 2 ; Wang, Muyang 3 ; Zhu, Ying; He, Zuhua;

作者机构： 1.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Plant Physiol & Ecol, Natl Key Lab Plant Mol Genet, Shanghai 200032, Peoples R China

2.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Plant Physiol & Ecol, Natl Key Lab Plant Mol Genet, Shanghai 200032, Peoples R China; Zhejiang Acad Agr Sci, Inst Vegetables, Hangzhou 310021, Peoples R China; Univ Nebraska, Dept Agron & Hort, Lincoln, NE 68583 USA

3.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Plant Physiol & Ecol, Natl Key Lab Plant Mol Genet,

期刊名称：PLANT PHYSIOLOGY （ 影响因子：8.34； 五年影响因子：8.972 ）

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收录情况： SCI

摘要： 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 (Arabidopsis thaliana), encodes a protein possessing 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 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 impaired different resistance-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 and basal defense components, whereas the auxin pathway was derepressed through up-regulating IAA biosynthesis and down-regulating auxin repressor genes. Taken together, our data reveal novel regulatory functions of GH3.5 in the plant-pathogen interaction.

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