title: Arabidopsis GH3.5 regulates salicylic acid-dependent and both NPR1-dependent and independent defense responses.
abstract: The cross-talk between plant disease resistance and development is fundamental to understanding systemic physiological processes during pathogen attack. Our previous study showed that the Arabidopsis GH3.5 gene acts as a bifunctional modulator of the salicylic acid (SA)-mediated resistance and the auxin-mediated susceptibility during the Arabidopsis-Pseudomonas syringae interaction as well as development. Here, we further study the role and mechanism of GH3.5 involved in the SA-dependent defense pathway. Transcript and histochemical analysis of the GH3.5 promoter::GUS reporter expression indicate that GH3.5 is expressed with a strong temporal and spatial manner with predominant expression in the divisional tissues. Upon bacterial challenge, GUS activity is induced in the junction tissue around the infiltrated zone with higher levels in the vasculature with a pattern different between the incompatible and compatible interactions. Exogenous SA application enhances disease resistance in the activation-tagged mutant gh3.5-1D, while the GH3.5-mediated defense enhancement is depleted in the SA deficient gh3.5-1D/NahG double mutant, indicating that GH3.5 modulates defense response through the SA-dependent pathway. Furthermore, bacterial growth in the gh3.5-1D/npr1 double mutant treated with SA indicates that GH3.5 enhances the SA-mediated defense response through both NPR1-dependent and independent pathways.
authors.affiliation: National Key Laboratory of Plant Molecular Genetics; Institute of Plant Physiology and Ecology; Shanghai Institutes for Biological Sciences; Chinese Academy of Sciences; Shanghai, China.
authors.forename: Zhongqin
authors.initials: Z
authors.lastname: Zhang
authors.forename: Muyang
authors.initials: M
authors.lastname: Wang
authors.forename: Zhimiao
authors.initials: Z
authors.lastname: Li
authors.forename: Qun
authors.initials: Q
authors.lastname: Li
authors.forename: Zuhua
authors.initials: Z
authors.lastname: He