Abstract
The bacterial pathogen Xanthomonas campestris pv. vesicatoria 85–10 (Xcv) translocates about 30 type-3 effector proteins (T3Es) into pepper plants (Capsicum annuum) to suppress plant immune responses. Among them is XopB which interferes with PTI, ETI and sugar-mediated defence responses, but the underlying molecular mechanisms and direct targets are unknown so far. Here, we examined the XopB-mediated suppression of plant defence responses in more detail. Infection of susceptible pepper plants with Xcv lacking xopB resulted in delayed symptom development compared to Xcv wild type infection concomitant with an increased formation of salicylic acid (SA) and expression of pathogenesis-related (PR) genes. Expression of xopB in Arabidopsis thaliana promoted the growth of the virulent Pseudomonas syringae pv. tomato (Pst) DC3000 strain. This was paralleled by a decreased SA-pool and a lower induction of SA-dependent PR gene expression. The expression pattern of early flg22-responsive marker genes indicated that MAPK signalling was not altered in the presence of XopB. However, XopB inhibited the flg22-triggered burst of reactive oxygen species (ROS). Consequently, the transcript accumulation of AtOXI1, a ROS-dependent marker gene, was reduced in xopB-expressing Arabidopsis plants as well as callose deposition. The lower ROS production correlated with a low level of basal and flg22-triggered expression of apoplastic peroxidases and the NADPH oxidase RBOHD. Conversely, deletion of xopB in Xcv caused a higher production of ROS in leaves of susceptible pepper plants. Together our results demonstrate that XopB modulates ROS responses and might thereby compromise plant defence.
Highlights
Plants respond to bacterial pathogens with a vast array of defence responses
Leaves inoculated with Xanthomonas campestris pv. vesicatoria (Xcv) wild type developed severe necrotic lesions 5 days post infection, while those infected with the Xcv ΔxopB deletion strain displayed less severe signs of necrosis at this time point (Fig 1A)
No phenotypic differences between wild type and transgenic plants were observed before treatment with ethanol. These results show that the type-3 effector proteins (T3Es) protein XopB causes severe phenotypic changes leading to cell death when ectopically expressed in A. thaliana suggesting that XopB may interfere with plant metabolism [38] and / or signalling
Summary
Plants respond to bacterial pathogens with a vast array of defence responses. Recognition of the invading pathogen is a prerequisite for the activation of the defence system and the successful inhibition of bacterial propagation. Plants have employed a two-tier defence system to combat microbial invaders [1,2,3]. The first layer of defence is triggered by the recognition of PLOS ONE | DOI:10.1371/journal.pone.0159107. The first layer of defence is triggered by the recognition of PLOS ONE | DOI:10.1371/journal.pone.0159107 July 11, 2016
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