Abstract

ABA is involved in plant responses to a broad range of pathogens and exhibits complex antagonistic and synergistic relationships with salicylic acid (SA) and ethylene (ET) signaling pathways, respectively. However, the specific receptor of ABA that triggers the positive and negative responses of ABA during immune responses remains unknown. Through a reverse genetic analysis, we identified that PYR1, a member of the family of PYR/PYL/RCAR ABA receptors, is transcriptionally upregulated and specifically perceives ABA during biotic stress, initiating downstream signaling mediated by ABA-activated SnRK2 protein kinases. This exerts a damping effect on SA-mediated signaling, required for resistance to biotrophic pathogens, and simultaneously a positive control over the resistance to necrotrophic pathogens controlled by ET. We demonstrated that PYR1-mediated signaling exerted control on a priori established hormonal cross-talk between SA and ET, thereby redirecting defense outputs. Defects in ABA/PYR1 signaling activated SA biosynthesis and sensitized plants for immune priming by poising SA-responsive genes for enhanced expression. As a trade-off effect, pyr1-mediated activation of the SA pathway blunted ET perception, which is pivotal for the activation of resistance towards fungal necrotrophs. The specific perception of ABA by PYR1 represented a regulatory node, modulating different outcomes in disease resistance.

Highlights

  • Pathogen recognition triggers the altered accumulation of three major defense hormones: salicylic acid (SA), jasmonic acid (JA), and ethylene (ET)

  • Resistance Enhancement of pyr1 Plants to Pseudomonas syringae DC3000 In marked contrast to the results shown above, the role of ABA in repressing plant immunity against the biotrophic pathogens P. syringae DC3000 has been previously documented [6,19,20,21]

  • We demonstrated that pyrabactin resistance 1 (PYR1) was pivotal and played a positive role in disease resistance to P. cucumerina since overexpression of PYR1 (i.e., PYR1-OE transgenic line) conferred significantly enhanced resistance

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Summary

Introduction

Pathogen recognition triggers the altered accumulation of three major defense hormones: salicylic acid (SA), jasmonic acid (JA), and ethylene (ET). While JA and ET interact synergistically to activate certain disease responses, the JA and ET pathways act at least independently or even antagonistically with respect to the SA-dependent pathway [4,5]. Antagonistic interactions between SA and JA hormone signaling networks have been characterized [6,7,8]. JA levels decline soon after SA begins to accumulate [9]; this, suggests that, in response to a pathogen that can induce synthesis of both SA and JA, cross-talk is used by the plant to adjust the response in favor of the more effective pathway (i.e., the SA-mediated pathway). Tradeoffs between plant defenses against pathogens with different lifestyles must be strictly regulated [4,17], implying the fine-tuned deployment of conserved defense signals in different plant-pathogen interactions

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