The sulfated laminarin triggers a stress transcriptome before priming the SA- and ROS-dependent defenses during grapevine's induced resistance against Plasmopara viticola.
The sulfated laminarin triggers a stress transcriptome before priming the SA- and ROS-dependent defenses during grapevine's induced resistance against Plasmopara viticola.
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DOI：
10.1371/journal.pone.0088145
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Poinssot B
中科院分区：
文献类型：
--
作者：
Gauthier A;Trouvelot S;Kelloniemi J;Frettinger P;Wendehenne D;Daire X;Joubert JM;Ferrarini A;Delledonne M;Flors V;Poinssot B
葡萄藤（葡萄属vinifera）易受多种病原菌的侵染，给世界范围内的葡萄栽培造成了重大损失。化学防治是可行的，但农业生态问题引起了人们对替代方法的兴趣，特别是在通过激发剂处理引发植物免疫方面。先前已经证明β-葡聚糖海带多糖（Lam）及其硫酸化衍生物（PS3）诱导葡萄藤对霜霉病（葡萄生霜霉病）的抗性。然而，如果Lam elevating经典的葡萄藤防御，如氧化爆发，病程相关（PR）蛋白和植物抗毒素的生产，PS3引发葡萄藤抗性通过一个知之甚少的引发现象。本研究的目的是确定PS3诱导的抗性的分子机制。为此目的，我们研究了i）在未感染的葡萄藤上由PS3处理触发的信号传导事件和转录组重编程，ii）在葡萄疫霉感染期间由PS3引发的葡萄藤免疫应答。我们的研究结果表明：i）PS3不能引起葡萄藤细胞中活性氧（ROS）的产生、胞浆Ca 2+浓度的变化、丝裂原活化蛋白激酶（MAPK）的激活，但触发了长时间持续的质膜去极化; ii）PS3和Lam具有共同的胁迫响应转录组谱，部分重叠水杨酸（SA）和茉莉酸（JA）依赖的转录组谱。接种葡萄疫霉后，PS3特异性地启动SA和ROS依赖的防御途径，导致葡萄藤诱导对这种生物营养型的抗性。有趣的是，药理学研究表明，质膜去极化和下游ROS的产生是PS3诱导的抗性的关键事件。
Grapevine (Vitis vinifera) is susceptible to many pathogens which cause significant losses to viticulture worldwide. Chemical control is available, but agro-ecological concerns have raised interest in alternative methods, especially in triggering plant immunity by elicitor treatments. The β-glucan laminarin (Lam) and its sulfated derivative (PS3) have been previously demonstrated to induce resistance in grapevine against downy mildew (Plasmopara viticola). However, if Lam elicits classical grapevine defenses such as oxidative burst, pathogenesis-related (PR)-proteins and phytoalexin production, PS3 triggered grapevine resistance via a poorly understood priming phenomenon. The aim of this study was to identify the molecular mechanisms of the PS3-induced resistance. For this purpose we studied i) the signaling events and transcriptome reprogramming triggered by PS3 treatment on uninfected grapevine, ii) grapevine immune responses primed by PS3 during P. viticola infection. Our results showed that i) PS3 was unable to elicit reactive oxygen species (ROS) production, cytosolic Ca2+ concentration variations, mitogen-activated protein kinase (MAPK) activation but triggered a long lasting plasma membrane depolarization in grapevine cells, ii) PS3 and Lam shared a common stress-responsive transcriptome profile that partly overlapped the salicylate- (SA) and jasmonate-(JA)-dependent ones. After P. viticola inoculation, PS3 specifically primed the SA- and ROS-dependent defense pathways leading to grapevine induced resistance against this biotroph. Interestingly pharmacological approaches suggested that the plasma membrane depolarization and the downstream ROS production are key events of the PS3-induced resistance.
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