Abstract
Nucleotide-binding domain and leucine-rich repeat-containing (NLR) proteins function as sensors that perceive pathogen molecules and activate immunity. In plants, the accumulation and activation of NLRs is regulated by SUPPRESSOR OF G2 ALLELE OF skp1 (SGT1). In this work, we found that an effector protein named RipAC, secreted by the plant pathogen Ralstonia solanacearum, associates with SGT1 to suppress NLR-mediated SGT1-dependent immune responses, including those triggered by another R. solanacearum effector, RipE1. RipAC does not affect the accumulation of SGT1 or NLRs, or their interaction. However, RipAC inhibits the interaction between SGT1 and MAP kinases, and the phosphorylation of a MAPK target motif in the C-terminal domain of SGT1. Such phosphorylation is enhanced upon activation of immune signaling and contributes to the activation of immune responses mediated by the NLR RPS2. Additionally, SGT1 phosphorylation contributes to resistance against R. solanacearum. Our results shed light onto the mechanism of activation of NLR-mediated immunity, and suggest a positive feedback loop between MAPK activation and SGT1-dependent NLR activation.
Highlights
The activation and suppression of plant immunity are key events that determine the outcome of the interaction between plants and bacterial pathogens
RipAC contributes to Ralstonia solanacearum infection It is well established that T3Es collectively play an essential role in the development of disease caused by most bacterial plant pathogens, including R. solanacearum (Deslandes and Genin, 2014)
Plant invasion by bacterial pathogens leads to the recognition of bacterial elicitors, either PAMPs or effectors, which, in turn, promotes the production and activation of additional immune receptors
Summary
The activation and suppression of plant immunity are key events that determine the outcome of the interaction between plants and bacterial pathogens. The detection of T3E activities through NLRs leads to the activation of immune responses, which effectively prevent pathogen proliferation (Chiang and Coaker, 2015) The outcome of these responses is named effector-triggered immunity (ETI), and, in certain cases, may cause a hypersensitive response (HR) that involves the collapse of plant cells. In an evolutionary response to this phenomenon, T3E activities have evolved to suppress ETI (Jones and Dangl, 2006), which in turn exposes bacterial pathogens to further events of effector recognition For these reasons, the interaction between plants and microbial pathogens is often considered an evolutionary ‘arms race’, where the specific combination of virulence activities and immune receptors in a certain pathogen-plant pair defines the outcome of the interaction (Jones and Dangl, 2006). The suppression of PTI by T3Es has been widely documented (Macho and Zipfel, 2015), reports about T3Es that suppress ETI, and their biochemical characterization, remain scarce
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