Activation of a COI1‐dependent pathway in Arabidopsis by Pseudomonas syringae type III effectors and coronatine

Abstract

SummaryGram-negative bacteria use a variety of virulence factors including phytotoxins, exopolysaccharides, effectors secreted by the type III secretion system, and cell-wall-degrading enzymes to promote parasitism in plants. However, little is known about how these virulence factors alter plant cellular responses to promote disease. In this study, we show that virulent Pseudomonas syringae strains activate the transcription of an Arabidopsis ethylene response factor (ERF) gene, RAP2.6, in a coronatine insensitive 1 (COI1)-dependent manner. A highly sensitive RAP2.6 promoter-®re¯y luciferase (RAP2.6-LUC) reporter line was developed to monitor activities of various bacterial virulence genes. Analyses of P. syringae pv. tomato DC3000 mutants indicated that both type III secretion system and the phytotoxin coronatine are required for RAP2.6 induction. We show that at least ®ve individual type III effectors, avirulence B (AvrB), AvrRpt2, AvrPphB, HopPtoK, and AvrPphE Pto , contributed to RAP2.6 induction. Gene-for-gene recognition was not involved in RAP2.6 induction because plants lacking RPM1 and RPS2 responded normally to AvrB and AvrRpt2 in RAP2.6 expression. Interestingly, the role of coronatine in RAP2.6 induction can be partially substituted by the addition of avrB in DC3000, suggesting that AvrB may mimic coronatine. These results suggest that P. syringae type III effectors and coronatine act by augmenting a COI1-dependent pathway to promote parasitism.

An Arabidopsis Plasma Membrane Proton ATPase Modulates JA Signaling and Is Exploited by the Pseudomonas syringae Effector Protein AvrB for Stomatal Invasion

“…This is consistent with our previous findings that bacterially delivered AvrB can substitute for COR function to enhance JA response gene expression (He et al, 2004;Cui et al, 2010).…”

“…We previously showed that AvrB can substitute COR to induce JA response genes (He et al, 2004). Because a major function of COR is to induce stomatal opening, this raises the possibility that AvrB may similarly promote stomatal opening.…”

“…We previously showed that AvrB can complement COR deficiency and induce JA response genes in plants in a RIN4-dependent manner (He et al, 2004;Cui et al, 2010). We sought to test if RIN4 was similarly required for avrB-induced stomatal virulence.…”

“…The AvrB-RIN4 interaction has been hypothesized to promote bacterial virulence in plants lacking RPM1 (Dangl and Jones, 2001;Kim et al, 2005), but direct evidence is lacking. Nonetheless, we have previously shown that AvrB can substitute COR to induce JA response gene expression in a manner dependent on COI1 and RIN4 (He et al, 2004;Shang et al, 2006;Cui et al, 2010). Whether the elevated JA signaling contributes to bacterial virulence remains unknown.…”

Effector MiSSP7 of the mutualistic fungus Laccaria bicolor stabilizes the Populus JAZ6 protein and represses jasmonic acid (JA) responsive genes

“…Because JAZ proteins are negative regulators of the JA signaling network, their degradation leads to transcriptional activation of plant defense networks within affected cells (6)(7)(8). Biotrophic pathogens have evolved methods of favoring JA signaling through the use of effector proteins because the outcomes of this hormonal pathway is considered less detrimental to their growth within plant tissues compared with defenses induced by other plant hormones [e.g., salicylic acid (SA)] (9)(10)(11)(12). Not all organisms attempting to colonize plant tissues, however, have adverse affects on plant health.…”