Viral-Induced Systemic Necrosis in Plants Involves Both Programmed Cell Death and the Inhibition of Viral Multiplication, Which Are Regulated by Independent Pathways
Viral-Induced Systemic Necrosis in Plants Involves Both Programmed Cell Death and the Inhibition of Viral Multiplication, Which Are Regulated by Independent Pathways
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DOI：
10.1094/mpmi-23-3-0283
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发表时间：
2010-03-01
影响因子：
3.5
通讯作者：
Namba, Shigetou
中科院分区：
文献类型：
--
作者：
Komatsu, Ken;Hashimoto, Masayoshi;Namba, Shigetou
抗性植物通过触发过敏反应（HR）对入侵的无毒植物病毒迅速作出反应。HR伴随着病毒增殖和程序性细胞死亡（PCD）的抑制，这两者都已在成功的病毒感染引发的全身性坏死中观察到。在这里，我们分析了信号转导途径的HR在抗性基因型植物和那些导致系统性坏死。我们发现，在烟草本塞姆，诱导亚洲车前花叶病毒（Plantago asiatica mosaic virus，PlAMV）感染，全身性坏死与PCD，生化特征，和基因表达模式的特征HR.The诱导坏死引起的PlAMV感染依赖于SGT1，RAR 1，和下游丝裂原活化蛋白激酶（MAPK）级联反应，涉及MAPKKK α和MEK 2。然而，尽管SGT1和RAR 1沉默导致PlAMV积累增加，但MAPKKK α-MEK 2级联的沉默不会。这一观察结果表明，即使在病毒感染诱导的全身性坏死中，病毒增殖也受到部分抑制，并且这种抑制需要SGT1和RAR 1，但不需要MAPKKK α-MEK 2级联。类似地，尽管SGT1和MAPKKK α对于Rx介导的马铃薯X病毒（PVX）HR都是必需的，但SGT1而不是MAPKKK α参与PVX增殖的抑制。这些结果表明，系统性坏死和HR包括PCD和病毒增殖的抑制，后者是通过独立于前者的未知途径诱导的。
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 MAPKKK alpha and MEK2. However, although SGT1 and RAR1 silencing led to an increased accumulation of PlAMV, silencing of the MAPKKK alpha-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 MAPKKK alpha-MEK2 cascade. Similarly, although both SGT1 and MAPKKK alpha were essential for the Rx-mediated HR to Potato virus X (PVX), SGT1 but not MAPKKK alpha 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.