Priller Johannes Peter Roman, Reid Stephen, Konein Patrick, Dietrich Petra, Sonnewald Sophia
Department of Biology, Division of Biochemistry, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany.
Department of Biology, Division of Molecular Plant Physiology, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany.
PLoS One. 2016 Jul 11;11(7):e0159107. doi: 10.1371/journal.pone.0159107. eCollection 2016.
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.
细菌性病原菌野油菜黄单胞菌辣椒斑点病致病型85-10（Xcv）向辣椒植株（辣椒）中转运约30种Ⅲ型效应蛋白（T3Es），以抑制植物免疫反应。其中的XopB会干扰植物的基础免疫（PTI）、效应子触发的免疫（ETI）以及糖介导的防御反应，但目前其潜在的分子机制和直接作用靶点尚不清楚。在此，我们更详细地研究了XopB介导的对植物防御反应的抑制作用。与野生型Xcv感染相比，用缺失xopB的Xcv感染易感辣椒植株，症状发展延迟，同时水杨酸（SA）的生成增加，病程相关（PR）基因的表达上调。在拟南芥中表达xopB可促进强致病力的丁香假单胞菌番茄致病型（Pst）DC3000菌株的生长。与此同时，SA库减少，SA依赖的PR基因表达的诱导水平降低。早期flg22反应性标记基因的表达模式表明，在存在XopB的情况下，丝裂原活化蛋白激酶（MAPK）信号传导未发生改变。然而，XopB抑制了flg22触发的活性氧（ROS）爆发。因此，在表达xopB的拟南芥植株中，ROS依赖的标记基因AtOXI1的转录积累以及胼胝质沉积均减少。较低的ROS产生与质外体过氧化物酶和NADPH氧化酶RBOHD的基础表达水平及flg22触发的表达水平较低相关。相反，Xcv中xopB的缺失导致易感辣椒植株叶片中ROS的产生增加。我们的研究结果共同表明，XopB可调节ROS反应，从而可能损害植物防御。
