A Prominent Role of the Flagellin Receptor FLAGELLIN-SENSING2 in Mediating Stomatal Response to Pseudomonas syringae pv tomato DC3000 in Arabidopsis    

Abstract

The FLAGELLIN-SENSING2 (FLS2) receptor kinase recognizes bacterial flagellin and initiates a battery of downstream defense responses to reduce bacterial invasion through stomata in the epidermis and bacterial multiplication in the apoplast of infected plants. Recent studies have shown that during Pseudomonas syringae pv tomato (Pst) DC3000 infection of Arabidopsis (Arabidopsis thaliana), FLS2-mediated immunity is actively suppressed by effector proteins (such as AvrPto and AvrPtoB) secreted through the bacterial type III secretion system (T3SS). We provide evidence here that T3SS effector-based suppression does not appear to be sufficient to overcome FLS2-based immunity during Pst DC3000 infection, but that the phytotoxin coronatine (COR) produced by Pst DC3000 also plays a critical role. COR-deficient mutants of Pst DC3000 are severely reduced in virulence when inoculated onto the leaf surface of wild-type Columbia-0 plants, but this defect was rescued almost fully in fls2 mutant plants. Although bacteria are thought to carry multiple microbe-associated molecular patterns, stomata of fls2 plants are completely unresponsive to COR-deficient mutant Pst DC3000 bacteria. The responses of fls2 plants were similar to those of the Arabidopsis G-protein alpha subunit1-3 mutant, which is defective in abscisic acid-regulated stomatal closure, but were distinct from those of the Arabidopsis non-expressor of PR genes1 mutant, which is defective in salicylic acid-dependent stomatal closure and apoplast defense. Epistasis analyses show that salicylic acid signaling acts upstream of abscisic acid signaling in bacterium-triggered stomatal closure. Taken together, these results suggest a particularly important role of FLS2-mediated resistance to COR-deficient mutant Pst DC3000 bacteria, and nonredundant roles of COR and T3SS effector proteins in the suppression of FLS2-mediated resistance in the Arabidopsis-Pst DC3000 interaction.

Biosynthesis and Defensive Function of N Δ-Acetylornithine, a Jasmonate-Induced Arabidopsis Metabolite

“…Since coronatine inhibits stomatal closure, thereby facilitating successful P. syringae infection (Melotto et al, 2006), these experiments were done under high humidity conditions, which promote stomatal opening and allow similar entry and growth of coronatine mutant and wild-type P. syringae. In the flagellin-sensitive2 (fls2) mutant background, where the stomatal closure response to P. syringae is compromised and coronatine is not required for entry (Zeng and He, 2010), there was also reduced N d -acetylornithine induction by coronatine-mutant P. syringae (see Supplemental Figure 6 online). Inoculation of wildtype Col-0 with DC3000 avrRpt2 (Whalen et al, 1991) and DC3000 avrRpm1 (Century et al, 1995) did not cause N dacetylornithine accumulation ( Figure 4A).…”

Pathogen-Associated Molecular Pattern-Triggered Immunity: Veni, Vidi…?

“…FLS2-mediated immunity is highly effective at the level of preinvasion, but also acts in postinvasive immunity as shown by flg22-induced local and systemic resistance (Zipfel, 2009;Zeng and He, 2010). A better time-wise and tissue-specific resolution is required to help understanding the contribution of perception of individual PAMPs and elicited responses.…”

The role of vacuolar processing enzymes in plant immunity

“…23,24 Stomatal closure can be triggered by pathogens, PAMPs and elicitors. 15,16,25,26 Therefore, the stomatal closure observed in such situations is an output of PTI.…”