College of Horticulture and Plant Protection, Joint International Research Laboratory of Agriculture and Agri-Product Safety, the Ministry of Education of China, Yangzhou University, Yangzhou, China.
Mol Plant Pathol. 2021 Dec;22(12):1668-1687. doi: 10.1111/mpp.13138. Epub 2021 Sep 22.
Systemic acquired resistance (SAR) is induced by pathogens and confers protection against a broad range of pathogens. Several SAR signals have been characterized, but the nature of the other unknown signalling by small metabolites in SAR remains unclear. Glutathione (GSH) has long been implicated in the defence reaction against biotic stress. However, the mechanism that GSH increases plant tolerance against virus infection is not entirely known. Here, a combination of a chemical, virus-induced gene-silencing-based genetics approach, and transgenic technology was undertaken to investigate the role of GSH in plant viral resistance in Nicotiana benthamiana. Tobacco mosaic virus (TMV) infection results in increasing the expression of GSH biosynthesis genes NbECS and NbGS, and GSH content. Silencing of NbECS or NbGS accelerated oxidative damage, increased accumulation of reactive oxygen species (ROS), compromised plant resistance to TMV, and suppressed the salicylic acid (SA)-mediated signalling pathway. Application of GSH or l-2-oxothiazolidine-4-carboxylic acid (a GSH activator) alleviated oxidative damage, decreased accumulation of ROS, elevated plant local and systemic resistance, enhanced the SA-mediated signalling pathway, and increased the expression of ROS scavenging-related genes. However, treatment with buthionine sulfoximine (a GSH inhibitor) accelerated oxidative damage, elevated ROS accumulation, compromised plant systemic resistance, suppressed the SA-mediated signalling pathway, and reduced the expression of ROS-regulating genes. Overexpression of NbECS reduced oxidative damage, decreased accumulation of ROS, increased resistance to TMV, activated the SA-mediated signalling pathway, and increased the expression of the ROS scavenging-related genes. We present molecular evidence suggesting GSH is essential for both local and systemic resistance of N. benthamiana to TMV through a differential modulation of SA and ROS.
系统获得性抗性 (SAR) 是由病原体诱导的，可对广泛的病原体提供保护。已经鉴定了几种 SAR 信号，但 SAR 中小代谢物的其他未知信号的性质尚不清楚。谷胱甘肽 (GSH) 长期以来一直被认为与生物胁迫的防御反应有关。然而，GSH 提高植物对病毒感染的耐受性的机制尚不完全清楚。在这里，采用化学物质、基于病毒诱导基因沉默的遗传学方法和转基因技术相结合，研究了 GSH 在 Nicotiana benthamiana 植物抗病毒中的作用。烟草花叶病毒 (TMV) 感染导致 GSH 生物合成基因 NbECS 和 NbGS 的表达增加，以及 GSH 含量增加。NbECS 或 NbGS 的沉默加速了氧化损伤，增加了活性氧 (ROS) 的积累，损害了植物对 TMV 的抗性，并抑制了水杨酸 (SA) 介导的信号通路。GSH 或 l-2-氧代噻唑烷-4-羧酸 (GSH 激活剂) 的应用缓解了氧化损伤，减少了 ROS 的积累，提高了植物的局部和系统抗性，增强了 SA 介导的信号通路，并增加了 ROS 清除相关基因的表达。然而，用丁硫氨酸亚砜 (GSH 抑制剂) 处理加速了氧化损伤，增加了 ROS 的积累，损害了植物的系统抗性，抑制了 SA 介导的信号通路，并降低了 ROS 调节基因的表达。NbECS 的过表达减轻了氧化损伤，减少了 ROS 的积累，提高了对 TMV 的抗性，激活了 SA 介导的信号通路，并增加了 ROS 清除相关基因的表达。我们提出了分子证据，表明 GSH 通过对 SA 和 ROS 的不同调节，对 N. benthamiana 对 TMV 的局部和系统抗性都是必需的。
