Plant Biology, Department of Biological and Environmental Sciences, University of Helsinki, PO Box 65 (Viikinkaari 1), FI-00014 Helsinki, Finland Institute of Technology, University of Tartu, Nooruse 1, Tartu 50411, Estonia.
Plant J. 2009 Apr;58(1):1-12. doi: 10.1111/j.1365-313X.2008.03756.x. Epub 2008 Dec 29.
Nitric oxide (NO) is involved together with reactive oxygen species (ROS) in the activation of various stress responses in plants. We have used ozone (O₃) as a tool to elicit ROS-activated stress responses, and to activate cell death in plant leaves. Here, we have investigated the roles and interactions of ROS and NO in the induction and regulation of O₃-induced cell death. Treatment with O₃ induced a rapid accumulation of NO, which started from guard cells, spread to adjacent epidermal cells and eventually moved to mesophyll cells. During the later time points, NO production coincided with the formation of hypersensitive response (HR)-like lesions. The NO donor sodium nitroprusside (SNP) and O₃ individually induced a large set of defence-related genes; however, in a combined treatment SNP attenuated the O₃ induction of salicylic acid (SA) biosynthesis and other defence-related genes. Consistent with this, SNP treatment also decreased O₃-induced SA accumulation. The O₃-sensitive mutant rcd1 was found to be an NO overproducer; in contrast, Atnoa1/rif1 (Arabidopsis nitric oxide associated 1/resistant to inhibition by FSM1), a mutant with decreased production of NO, was also O₃ sensitive. This, together with experiments combining O₃ and the NO donor SNP suggested that NO can modify signalling, hormone biosynthesis and gene expression in plants during O₃ exposure, and that a functional NO production is needed for a proper O₃ response. In summary, NO is an important signalling molecule in the response to O₃.
一氧化氮 (NO) 与活性氧物质 (ROS) 一起参与植物各种应激反应的激活。我们使用臭氧 (O₃) 作为一种工具来引发 ROS 激活的应激反应，并在植物叶片中激活细胞死亡。在这里，我们研究了 ROS 和 NO 在臭氧诱导的细胞死亡的诱导和调节中的作用和相互关系。O₃ 处理诱导了 NO 的快速积累，该过程始于保卫细胞，扩散到相邻的表皮细胞，最终移动到叶肉细胞。在稍后的时间点，NO 的产生与过敏反应 (HR) 样病变的形成同时发生。一氧化氮供体硝普钠 (SNP) 和 O₃ 各自诱导了一大组防御相关基因；然而，在联合处理中，SNP 减弱了 O₃ 诱导的水杨酸 (SA) 生物合成和其他防御相关基因的表达。与之一致的是，SNP 处理也降低了 O₃ 诱导的 SA 积累。发现 O₃ 敏感突变体 rcd1 是一个过度产生 NO 的突变体；相比之下，Atnoa1/rif1（拟南芥一氧化氮相关 1/抗 FSM1 抑制），一个 NO 产生减少的突变体，也对 O₃ 敏感。这与结合 O₃ 和 NO 供体 SNP 的实验一起表明，NO 可以在植物暴露于 O₃ 期间修饰信号、激素生物合成和基因表达，并且需要功能性的 NO 产生才能进行适当的 O₃ 反应。总之，NO 是对 O₃ 反应的重要信号分子。
