老文章新讨论-系统性坏死与过敏性坏死（HR）
Komatsu等2010年在MPMI上面发表了题为Viral-Induced Systemic Necrosis in Plants InvolvesBoth Programmed Cell Death and the Inhibitionof Viral Multiplication, Which Are Regulatedby Independent Pathways 的文章，文中在系统性坏死植物中发现类似于过敏性坏死反应的一些特性，例如PR1a, SGT1，RAR1等基因表达及其作用。但最终结论是系统性坏死和过敏性坏死反应都有PCD和抑制病毒繁殖的特点，但HR拥有自己特殊的途径。
希望大家聊聊自己的看法。怎么来看系统性坏死和过敏性坏死反应。
原文摘要：
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 MAPKKKα and MEK2. However, although SGT1 and RAR1 silencing led to an increased accumulation of PlAMV, silencing of the MAPKKKα-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 MAPKKKα-MEK2 cascade. Similarly, although both SGT1 and MAPKKKα were essential for the Rx-mediated HR to Potato virus X (PVX), SGT1 but not MAPKKKα 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.
过敏性坏死过程中包括细胞程序性死亡，和抑制病毒繁殖，激发植物抗性相关的基因，但事情反过来是否也成立呢？
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