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首页> 外文期刊>Journal of Experimental Botany >Modulation of cellular redox status by thiamine-activated NADPH oxidase confers Arabidopsis resistance to Sclerotinia sclerotiorum
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Modulation of cellular redox status by thiamine-activated NADPH oxidase confers Arabidopsis resistance to Sclerotinia sclerotiorum

机译：硫胺素激活的NADPH氧化酶对细胞氧化还原状态的调节赋予拟南芥对核盘菌核盘菌的抗性

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摘要

Sclerotinia sclerotiorum can initially suppress host oxidative burst to aid infection establishment, but later promotes reactive oxygen species (ROS) generation as proliferation advances. Here, it was shown that the cellular redox status can be modulated by thiamine to protect Arabidopsis thaliana against Sclerotinia at the early stages of infection. The initial inhibition of host ROS generation by Sclerotinia-secreted oxalate could effectively be alleviated by thiamine. Thiamine pre-treatment and subsequent wild-type Sclerotinia invasion induced an increase of ascorbate peroxidase activity concomitant with decreased ascorbate/dehydroascorbate ratios, which led to the cellular transition towards oxidative status in infected tissues. Particularly, it was observed that wild-type Sclerotinia, but not oxalate-deficient A2 mutant, could suppress the activity of NADPH oxidase (NOX), which might be an important mechanism underlying the early inhibition of ROS burst. Nevertheless, thiamine pre-treatment followed by wild-type Sclerotinia infection promoted NOX-derived ROS accumulation. Further studies showed that cytosolic Ca-2 and staurosporine-sensitive protein kinase(s) participated in thiamine-induced activation of NOX. Moreover, thiamine-induced tissue defence responses including callose/lignin deposition and stomatal closure were closely correlated with NOX-derived ROS generation. Additionally, studies with Brassica species indicated that the regulation of thiamine is largely conserved upon Sclerotinia infection. Collectively, it was concluded that thiamine reverses the initial reducing status through activating NOX-dependent ROS signalling to perturb the disease progress of Sclerotinia.
机译：核盘菌菌核菌最初可以抑制宿主的氧化爆发，以帮助感染的建立，但后来随着增殖的发展促进了活性氧（ROS）的产生。在这里，表明了在感染的早期阶段，硫胺素可以调节细胞的氧化还原状态，以保护拟南芥免受菌核病的侵害。硫胺素可以有效地减轻菌核菌分泌草酸盐对宿主ROS产生的最初抑制作用。硫胺素预处理和随后的野生型核盘菌入侵导致抗坏血酸过氧化物酶活性增加，同时抗坏血酸/脱氢抗坏血酸比率降低，从而导致感染组织的细胞向氧化状态过渡。特别是，观察到野生型菌核菌，但不是草酸盐缺陷型A2突变体，可以抑制NADPH氧化酶（NOX）的活性，这可能是早期抑制ROS爆发的重要机制。尽管如此，硫胺素预处理后再进行野生型核盘菌感染仍可促进NOX引起的ROS积累。进一步的研究表明，胞浆Ca-2和星形孢菌素敏感性蛋白激酶参与了硫胺素诱导的NOX活化。此外，硫胺素诱导的组织防御反应（包括call /木质素沉积和气孔关闭）与NOX衍生的ROS产生密切相关。另外，对芸苔属的研究表明硫胺素的调节在巩膜菌感染后很大程度上保持。总的来说，得出的结论是，硫胺素通过激活依赖于NOX的ROS信号来干扰菌核病的病情发展，从而逆转最初的还原状态。

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