Department of Horticulture, Huajiachi Campus, Zhejiang University, P. R. China.
Mol Plant Microbe Interact. 2010 Jan;23(1):39-48. doi: 10.1094/MPMI-23-1-0039.
The role of mitochondrial alternative oxidase (AOX) and the relationship between AOX and nitric oxide (NO) in virus-induced systemic defense to Tobacco mosaic virus (TMV) were investigated in susceptible tomato (Solanum lycopersicum) plants. TMV inoculation to the lower leaves induced a rapid NO synthesis and AOX activation in upper uninoculated leaves as early as 0.5 day postinoculation. Application of exogenous potassium cyanide (KCN, a cytochrome pathway inhibitor) at nonlethal concentrations and NO donor diethylamine NONOate (DEA/NO) to the upper uninoculated leaves greatly induced accumulation of AOX transcript, reduced TMV viral RNA accumulation, and increased the leaf photochemical quantum yield at photosystem II. Pretreatment with NO scavenger almost completely blocked TMV-induced AOX induction and substantially increased TMV susceptibility. Salicylhydroxamic acid (SHAM, an AOX inhibitor) pretreatment reduced the DEA/NO-induced cyanide-resistant respiration and partially compromised induced resistance to TMV. Conversely, KCN and SHAM pretreatment had very little effect on generation of NO, and pretreatment with NO scavenger did not affect KCN-induced AOX induction and TMV resistance. These results suggest that TMV-induced NO generation acts upstream and mediates AOX induction which, in turn, induces mitochondrial alternative electron transport and triggers systemic basal defense against the viral pathogen.
研究了线粒体交替氧化酶（AOX）在烟草花叶病毒（TMV）诱导的系统防御中的作用，以及 AOX 与一氧化氮（NO）之间的关系，研究对象为易感番茄（Solanum lycopersicum）植株。TMV 接种到下叶后，最早在接种后 0.5 天，上叶中就会迅速合成 NO 和激活 AOX。将非致死浓度的细胞色素途径抑制剂氰化钾（KCN）和一氧化氮供体二乙胺 NONOate（DEA/NO）应用于上叶未接种部位，会极大地诱导 AOX 转录物的积累，减少 TMV 病毒 RNA 的积累，并增加光系统 II 的叶片光化学量子产量。NO 清除剂预处理几乎完全阻断了 TMV 诱导的 AOX 诱导，大大增加了 TMV 的易感性。水杨羟肟酸（SHAM，AOX 抑制剂）预处理降低了 DEA/NO 诱导的氰化物抗性呼吸，并部分削弱了对 TMV 的诱导抗性。相反，KCN 和 SHAM 预处理对 NO 的生成几乎没有影响，而 NO 清除剂预处理也不影响 KCN 诱导的 AOX 诱导和 TMV 抗性。这些结果表明，TMV 诱导的 NO 生成作用于上游，并介导 AOX 诱导，进而诱导线粒体替代电子传递，并引发针对病毒病原体的系统基础防御。
