Antagonism between salicylic and abscisic acid reflects early host–pathogen conflict and moulds plant defence responses

Abstract

SUMMARYThe importance of phytohormone balance is increasingly recognized as central to the outcome of plantpathogen interactions. Recently it has been demonstrated that abscisic acid signalling pathways are utilized by the bacterial phytopathogen Pseudomonas syringae to promote pathogenesis. In this study, we examined the dynamics, inter-relationship and impact of three key acidic phytohormones, salicylic acid, abscisic acid and jasmonic acid, and the bacterial virulence factor, coronatine, during progression of P. syringae infection of Arabidopsis thaliana. We show that levels of SA and ABA, but not JA, appear to play important early roles in determining the outcome of the infection process. SA is required in order to mount a full innate immune responses, while bacterial effectors act rapidly to activate ABA biosynthesis. ABA suppresses inducible innate immune responses by down-regulating SA biosynthesis and SA-mediated defences. Mutant analyses indicated that endogenous ABA levels represent an important reservoir that is necessary for effector suppression of plant-inducible innate defence responses and SA synthesis prior to subsequent pathogeninduced increases in ABA. Enhanced susceptibility due to loss of SA-mediated basal resistance is epistatically dominant over acquired resistance due to ABA deficiency, although ABA also contributes to symptom development. We conclude that pathogen-modulated ABA signalling rapidly antagonizes SA-mediated defences. We predict that hormonal perturbations, either induced or as a result of environmental stress, have a marked impact on pathological outcomes, and we provide a mechanistic basis for understanding priming events in plant defence.

Abscisic Acid Has a Key Role in Modulating Diverse Plant-Pathogen Interactions

“…These experiments were repeated twice with similar outcomes. ABA biosynthesis and signaling pathways may be targeted by P. syringae TTSS effectors to suppress the plant defense response (de Torres-Zabala et al, 2007). Our study on the cds2-1D mutant showed that activation of ABA biosynthesis weakened several plant defense systems against bacterial infection.…”

“…Previous studies showed that treatment of Arabidopsis plants with flg22 peptide or the nonpathogenic hrcC strain of Pst may lead to callose-associated cell wall modification (Gó mez-Gó mez et al, 1999; Hauck et al, 2003), and this extracellular defense response is suppressed by wild-type pathogenic bacteria or overexpression in planta of bacterial TTSS effectors (Hauck et al, 2003;Kim et al, 2005). Recent data showed that wild-type Pst enhances callose deposition in Arabidopsis mutants impaired in ABA biosynthesis or signaling, and exogenous ABA suppresses flg22 peptide induced callose deposition in wild-type Arabidopsis seedlings (de Torres-Zabala et al, 2007Clay et al, 2009), indicating a negative role of ABA in activation of callose deposition. However, early studies also showed that an ABA-dependent defense pathway mediates priming of callose deposition in b-amino-butyric acid (BABA)-induced resistance against necrotrophic pathogens (Ton and Mauch-Mani, 2004).…”

Mechanisms and ecological implications of plant‐mediated interactions between belowground and aboveground insect herbivores

“…1) (Anderson et al 2004;Lorenzo and Solano 2005;Pre´et al 2008). Moreover, interactions of both ABA and ET with other molecular players of the signaling network have been reported and thus these phytohormones may affect plant defenses against insect herbivores (de Torres-Zabala et al 2009;Jiang et al 2010;Kazan and Manners 2012;Pieterse et al 2012). The role of ABA and ET in BG-AG interactions has been shown (Jackson 1997;Erb et al 2009a).…”

The Pseudomonas syringae Type III Effector AvrRpt2 Promotes Pathogen Virulence via Stimulating Arabidopsis Auxin/Indole Acetic Acid Protein Turnover

“…Free auxin levels increase in plants infected with P. syringae or Xanthomonas spp., and application of exogenous auxin promotes disease susceptibility (O'Donnell et al, 2003;Chen et al, 2007;Wang et al, 2007). Inappropriate activation of ABA biosynthesis and signaling disrupts plant resistance to several pathogens (de Torres Zabala et al, 2009;Fan et al, 2009). Brassinosteroids unidirectionally suppress plant PTI signaling at multiple levels (Albrecht et al, 2012;Belkhadir et al, 2012).…”