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

• Published in: Plant physiology (Bethesda) 2007-10, Vol.145 (2), p.450-464
• Main Authors: Zhang, Zhongqin, Li, Qun, Li, Zhimiao, Staswick, Paul E, Wang, Muyang, Zhu, Ying, He, Zuhua
• Format: Article
• Language: English
• Subjects: Arabidopsis - genetics; Arabidopsis - metabolism; Arabidopsis - microbiology; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Arabidopsis thaliana; Auxins; Disease resistance; Gene Expression Profiling; Gene expression regulation; Gene Expression Regulation, Plant; Genes; Host-Pathogen Interactions; Indoleacetic Acids - metabolism; Infections; Insulin antibodies; Leaves; Ligases - genetics; Ligases - metabolism; Mutation; Pathogens; Plant Diseases - microbiology; Plant growth; Plants; Plants Interacting with Other Organisms; Pseudomonas syringae - physiology; Salicylic Acid - metabolism; Signal Transduction - physiology; Transcription, Genetic
• ISSN: 0032-0889; 1532-2548; 1532-2548
• DOI: 10.1104/pp.107.106021

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.