The suppressor of transgene RNA silencing encoded by Cucumber mosaic virus interferes with salicylic acid-mediated virus resistance

The suppressor of transgene RNA silencing encoded by Cucumber mosaic virus interferes with salicylic acid-mediated virus resistance
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DOI:
10.1094/mpmi.2001.14.6.715
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发表时间:
2001-06-01
影响因子:
3.5
通讯作者:
Ding, SW
Ding, SW
中科院分区:
生物学2区
文献类型:
--
作者:
Ji, LH;Ding, SW

文献摘要

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相似文献

黄瓜花叶病毒(CMV)编码的2b蛋白(Cmv2b)是抑制本氏烟草(Nicotiana benthamiana)中转基因RNA沉默的核蛋白。Cmv2b是一个重要的毒力决定因子,但不是系统传播所必需的。在此,我们报道了Cmv2b在老N.在用水杨酸(SA)预处理的幼苗中。无论是CMV还是烟草花叶病毒基因组中Cmv2b的表达都显著降低了SA对接种叶片和系统叶片中病毒积累的抑制作用。Cmv2b的表达和减少SA依赖性的替代氧化酶基因的诱导,最近提出的SA调节的抗病毒防御的一个组成部分之间表现出密切的相关性。这些结果共同揭示了一种新的活性Cmv2b在抑制SA介导的病毒抗性。我们用了N。表达细菌nahG转基因的烟草品系,该转基因降解SA以提供烟草中Cmv2b敏感的抗病毒防御机制的证据,其中SA充当正修饰剂而不是必需组分。我们提出SA通过增强Cmv2b靶向的RNA沉默抗病毒防御来诱导病毒抗性。
The Cucumber mosaic virus (CMV)-encoded 2b protein (Cmv2b) is a nuclear protein that suppresses transgene RNA silencing in Nicotiana benthamiana. Cmv2b is an important virulence determinant but nonessential for systemic spread ill N. glutinosa, in contrast to its indispensable role for systemic infections in cucumber, Here, we report that Cmv2b became essential for systemic infections in older N. glutinosa plants or in young seedlings pretreated with salicylic acid (SA). Expression of Cmv2b from the genome of either CMV or Tobacco mosaic virus significantly reduced the inhibitory effect of SA on virus accumulation in inoculated leaves and systemic leaves. A close correlation is demonstrated between Cmv2b expression and a reduced SA-dependent induction of the alternative oxidase gene, a component of the recently proposed SA-regulated antiviral defense, These results collectively reveal a novel activity of Cmv2b in the inhibition of SA-mediated virus resistance. We used a N. tabacum line expressing a bacterial nahG transgene that degrades SA to provide evidence for a Cmv2b-sensitive antiviral defense mechanism in tobacco in which SA acts as a positive modifier but not as an essential component. We propose that SA induces virus resistance by potentiating a RNA-silencing antiviral defense that is targeted by Cmv2b.