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. 2008 Aug;3(8):537-42.
doi: 10.4161/psb.3.8.5748.

Arabidopsis GH3.5 regulates salicylic acid-dependent and both NPR1-dependent and independent defense responses

Zhongqin Zhang  1 , Muyang Wang, Zhimiao Li, Qun Li, Zuhua He
Affiliations

Arabidopsis GH3.5 regulates salicylic acid-dependent and both NPR1-dependent and independent defense responses

Zhongqin Zhang et al. Plant Signal Behav. 2008 Aug.

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.

Keywords: GH3.5; NPR1; NahG; Pseudomonas syringae; defense response; double mutants; salicylic acid.

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Figures

Figure 1
Figure 1
Expression pattern of GH3.5. (A) Northern blot analysis of GH3.5 in different tissues of Col-0. (B) GUS activity in 7-day-old seedling of the GH3.5-GUS transgenic plant. (C–E) GUS activity during lateral root development in the GH3.5-GUS plant. (F) GUS activity in buds of the GH3.5-GUS plant. (G) GUS activity in the blooming flower of the GH3.5-GUS plant.
Figure 2
Figure 2
SA-induced disease resistance in Col-0 and gh3.5-1D. (A) Disease symptom of Pst DC3000 in mock and SA-treated Col-0 (left) and gh3.5-1D (+/−) (right). Five-week-old plants of the wildtype and mutants were sprayed with 1 mM SA and further inoculated with Pst DC3000 at a dose of 105 cfu ml−1 (OD600 = 0.0002). All controls were infiltrated with 10 mM MgCl2 for mock inoculation. Photos were taken at 3 dpi. Similar results were observed in two independent experiments. (B) Growth of Pst DC3000 in SA-treated leaves of Col-0 and gh3.5-1D. Bacterial growth assay was performed at 0 and 3 days after inoculation in Col-0 and gh3.5-1D (+/−). All values are means ± SE (n = 6). The SA-induced resistance was significantly stronger (p < 0.05) in gh3.5-1D than the wldtype. cfu, colony-forming units. Similar results were observed in two independent experiments.
Figure 3
Figure 3
Histochemical assay of the expression pattern of the GH3.5-GUS reporter in responses to pathogen. (A) Induction of the GH3.5-GUS fusion reporter by Pst DC3000(avrRpt2) and Pst DC3000 at 107 cfu ml−1 at 3 dpi. FI, filter-infected areas. (B) Induction of the GH3.5-GUS fusion reporter by Psm(avrRpm1) and Psm at 107 cfu ml−1 at 3 dpi. Leaves were infiltrated with 10 mM MgCl2 for mock inoculation (A and B).
Figure 4
Figure 4
GH3.5 modulates SA-dependent defense response. (A) Northern blot analysis of PR-1 induction by exogenous application of SA (0.5 mM) over a time course of 0 to 48 h after treatment in gh3.5-1D heterozygous (gh3.5-1D+/−) and homozygous (gh3.5-1D−/−) plants, in comparison with Col-0 plants. The experiment was biologically repeated once. (B) Expression of PR-1 in NahG, gh3.5-1D/NahG double mutant and gh3.5-1D plants after infection with Psm(avrRpm1) at 107 cfu ml−1. Leaves were collected at 0 and 48 hpi. The experiments were repeated once with similar results. (C) Growth of Pst DC3000 in Col-0, NahG and gh3.5-1D/NahG plants after pre-treatment with SA (1 mM) or buffer (mock). Bacterial titers were repeated twice with similar results. All values are the mean ± SE (n = 6).
Figure 5
Figure 5
SA-independent induction of GH3.5 and NPR1-dependent and independent SA-induced defense. (A) The induction of GH3.5 by Psm(avrRpm1) at 107 cfu ml−1 in Col-0, NahG, sid2-2 and npr1-1 plants, indicating that the GH3.5 induction was not affected by SA deficiency in these mutants. (B) Growth of Pst DC3000 in Col-0, npr1 and gh3.5-1D/npr1 plants after pre-treatment with SA (1 mM) or buffer. Bacterial titers were repeated twice with similar results. All values are the mean ± SE (n = 6).
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