Laboratory Of Plant Pathology, Department Of Agricultural And Environmental Biology, Graduate School Of Agricultural And Life Sciences, The University Of Tokyo, Tokyo, Japan.
Mol Plant Microbe Interact. 2010 Mar;23(3):283-93. doi: 10.1094/MPMI-23-3-0283.
Resistant plants respond rapidly to invading avirulent plant viruses by triggering a hypersensitive response (HR). An HR is accompanied by a restraint of virus multiplication and programmed cell death (PCD), both of which have been observed in systemic necrosis triggered by a successful viral infection. Here, we analyzed signaling pathways underlying the HR in resistance genotype plants and those leading to systemic necrosis. We show that systemic necrosis in Nicotiana benthamiana, induced by Plantago asiatica mosaic virus (PlAMV) infection, was associated with PCD, biochemical features, and gene expression patterns that are characteristic of HR. The induction of necrosis caused by PlAMV infection was dependent on SGT1, RAR1, and the downstream mitogen-activated protein kinase (MAPK) cascade involving MAPKKKalpha and MEK2. However, although SGT1 and RAR1 silencing led to an increased accumulation of PlAMV, silencing of the MAPKKKalpha-MEK2 cascade did not. This observation indicates that viral multiplication is partly restrained even in systemic necrosis induced by viral infection, and that this restraint requires SGT1 and RAR1 but not the MAPKKKalpha-MEK2 cascade. Similarly, although both SGT1 and MAPKKKalpha were essential for the Rx-mediated HR to Potato virus X (PVX), SGT1 but not MAPKKKalpha was involved in the restraint of PVX multiplication. These results suggest that systemic necrosis and HR consist of PCD and a restraint of virus multiplication, and that the latter is induced through unknown pathways independent from the former.
抗性植物通过触发过敏反应（HR）快速响应入侵的无毒植物病毒。HR 伴随着病毒复制的抑制和程序性细胞死亡（PCD），这两者都在成功的病毒感染引发的系统坏死中观察到。在这里，我们分析了抗性基因型植物中 HR 的信号通路以及导致系统坏死的信号通路。我们表明，由 Plantago asiatica mosaic virus (PlAMV) 感染诱导的 Nicotiana benthamiana 系统坏死与 PCD、生化特征和基因表达模式有关，这些特征与 HR 有关。PlAMV 感染诱导坏死的诱导依赖于 SGT1、RAR1 和涉及 MAPKKKalpha 和 MEK2 的下游丝裂原激活蛋白激酶（MAPK）级联。然而，尽管 SGT1 和 RAR1 的沉默导致 PlAMV 的积累增加，但 MAPKKKalpha-MEK2 级联的沉默并没有。这一观察表明，即使在病毒感染诱导的系统坏死中，病毒复制也受到部分抑制，这种抑制需要 SGT1 和 RAR1，但不需要 MAPKKKalpha-MEK2 级联。同样，尽管 SGT1 和 MAPKKKalpha 对于 Rx 介导的对 Potato virus X (PVX) 的 HR 都是必不可少的，但 SGT1 而不是 MAPKKKalpha 参与了对 PVX 复制的抑制。这些结果表明，系统坏死和 HR 由 PCD 和病毒复制的抑制组成，后者是通过独立于前者的未知途径诱导的。
