Király Lóránt, Albert Réka, Zsemberi Orsolya, Schwarczinger Ildikó, Hafez Yaser Mohamed, Künstler András
Department of Plant Pathophysiology, Plant Protection Institute, Centre for Agricultural Research, Eötvös Loránd Research Network (ELKH), H-1022 Budapest, Hungary.
Division of Toxicology, Wageningen University & Research, 6708 WE Wageningen, The Netherlands.
Phytopathology. 2021 Oct;111(10):1870-1884. doi: 10.1094/PHYTO-12-20-0540-R. Epub 2021 Nov 3.
Here we show that in tobacco ( cultivar Samsun NN ) the development of gene-mediated, symptomless, extreme resistance to (PVX) is preceded by an early, intensive accumulation of the reactive oxygen species (ROS) superoxide (O·), evident between 1 and 6 h after inoculation and associated with increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activities. This suggests a direct contribution of this ROS to virus restriction during symptomless, extreme resistance. Superoxide inhibition in PVX-inoculated leaves by infiltration of antioxidants (superoxide dismutase [SOD] and catalase [CAT]) partially suppresses extreme resistance in parallel with the appearance of localized leaf necrosis resembling a hypersensitive resistance (HR) response. F progeny from crosses of and ferritin overproducer (deficient in production of the ROS OH·) tobaccos also display a suppressed extreme resistance to PVX, because significantly increased virus levels are coupled to HR, suggesting a role of the hydroxyl radical (OH·) in this symptomless antiviral defense. In addition, treatment of PVX-susceptible tobacco with a superoxide-generating agent (riboflavin/methionine) results in HR-like symptoms and reduced PVX titers. Finally, by comparing defense responses during PVX-elicited symptomless, extreme resistance and HR-type resistance elicited by , we conclude that defense reactions typical of an HR (e.g., induction of cell death/ROS-regulator genes and antioxidants) are early and transient in the course of extreme resistance. Our results demonstrate the contribution of early accumulation of ROS (superoxide, OH·) in limiting PVX replication during symptomless extreme resistance and support earlier findings that virus-elicited HR represents a delayed, slower resistance response than symptomless, extreme resistance.
我们在此表明，在烟草（品种Samsun NN）中，基因介导的对马铃薯X病毒（PVX）无症状的极端抗性的发展之前，活性氧（ROS）超氧化物（O·）会早期大量积累，在接种后1至6小时明显可见，且与烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶活性增加相关。这表明这种ROS在无症状的极端抗性过程中对病毒限制有直接作用。通过浸润抗氧化剂（超氧化物歧化酶[SOD]和过氧化氢酶[CAT]）抑制PVX接种叶片中的超氧化物，部分抑制了极端抗性，同时出现了类似于过敏反应（HR）的局部叶片坏死。野生型和铁蛋白过量产生（缺乏ROS羟基自由基[OH·]产生）烟草杂交的F子代对PVX的极端抗性也受到抑制，因为病毒水平显著增加与HR相关，这表明羟基自由基（OH·）在这种无症状的抗病毒防御中起作用。此外，用超氧化物生成剂（核黄素/蛋氨酸）处理对PVX敏感的烟草会导致类似HR的症状并降低PVX滴度。最后，通过比较PVX引发的无症状极端抗性和丁香假单胞菌引发的HR型抗性过程中的防御反应，我们得出结论，HR典型的防御反应（如细胞死亡/ROS调节基因和抗氧化剂的诱导）在极端抗性过程中是早期且短暂的。我们的结果证明了ROS（超氧化物、OH·）早期积累在无症状极端抗性期间限制PVX复制中的作用，并支持了早期的发现，即病毒引发的HR代表了一种比无症状极端抗性延迟、缓慢的抗性反应。
