Van Bockhaven Jonas, Spíchal Lukáš, Novák Ondřej, Strnad Miroslav, Asano Takayuki, Kikuchi Shoshi, Höfte Monica, De Vleesschauwer David
Laboratory of Phytopathology, Faculty of Bioscience Engineering, Ghent University, B-9000, Ghent, Belgium.
New Phytol. 2015 Apr;206(2):761-73. doi: 10.1111/nph.13270. Epub 2015 Jan 27.
Although numerous studies have shown the ability of silicon (Si) to mitigate a wide variety of abiotic and biotic stresses, relatively little is known about the underlying mechanism(s). Here, we have investigated the role of hormone defense pathways in Si-induced resistance to the rice brown spot fungus Cochliobolus miyabeanus. To delineate the involvement of multiple hormone pathways, a multidisciplinary approach was pursued, combining exogenous hormone applications, pharmacological inhibitor experiments, time-resolved hormone measurements, and bioassays with hormone-deficient and/or -insensitive mutant lines. Contrary to other types of induced resistance, we found Si-induced brown spot resistance to function independently of the classic immune hormones salicylic acid and jasmonic acid. Our data also rule out a major role of the abscisic acid (ABA) and cytokinin pathways, but suggest that Si mounts resistance to C. miyabeanus by preventing the fungus from hijacking the rice ethylene (ET) machinery. Interestingly, rather than suppressing rice ET signaling per se, Si probably interferes with the production and/or action of fungal ET. Together our findings favor a scenario whereby Si induces brown spot resistance by disarming fungal ET and argue that impairment of pathogen virulence factors is a core resistance mechanism underpinning Si-induced plant immunity.
尽管大量研究表明硅（Si）能够减轻多种非生物和生物胁迫，但对其潜在机制的了解相对较少。在此，我们研究了激素防御途径在硅诱导的水稻对稻瘟病菌（Cochliobolus miyabeanus）抗性中的作用。为了阐明多种激素途径的参与情况，我们采用了多学科方法，结合外源激素处理、药理学抑制剂实验、激素的时间分辨测量以及对激素缺陷和/或不敏感突变体品系的生物测定。与其他类型的诱导抗性相反，我们发现硅诱导的稻瘟病抗性独立于经典免疫激素水杨酸和茉莉酸发挥作用。我们的数据也排除了脱落酸（ABA）和细胞分裂素途径的主要作用，但表明硅通过阻止真菌劫持水稻乙烯（ET）机制来增强对稻瘟病菌的抗性。有趣的是，硅可能不是直接抑制水稻ET信号传导，而是干扰真菌ET的产生和/或作用。我们的研究结果共同支持了这样一种情况，即硅通过解除真菌ET的作用来诱导稻瘟病抗性，并认为病原体毒力因子的受损是硅诱导植物免疫的核心抗性机制。
