Two plant viral suppressors of silencing require the ethylene-inducible host transcription factor RAV2 to block RNA silencing.
Two plant viral suppressors of silencing require the ethylene-inducible host transcription factor RAV2 to block RNA silencing.
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DOI：
10.1371/journal.ppat.1000729
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发表时间：
2010-01-15
期刊：
影响因子：
6.7
通讯作者：
Vance V
中科院分区：
文献类型：
--
作者：
Endres MW;Gregory BD;Gao Z;Foreman AW;Mlotshwa S;Ge X;Pruss GJ;Ecker JR;Bowman LH;Vance V
RNA沉默是在病毒感染期间激活的相互关联的防御反应网络中的高度保守的途径。作为一种反防御，许多植物病毒编码阻止沉默的蛋白质，通常也干扰内源性小RNA途径。然而，病毒抑制因子的作用机制还不清楚，宿主因子在该过程中的作用才刚刚开始出现。在这里，我们报告说，乙烯诱导的转录因子RAV 2的抑制RNA沉默所需的两个无关的植物病毒蛋白，马铃薯Y病毒HC-Pro和carmovirus P38。使用发夹转基因沉默系统，我们发现两种病毒抑制因子都需要RAV 2来阻断初级siRNA的活性，而传递性沉默的抑制是RAV 2独立的。RAV 2也是转基因植物中许多HC-Pro介导的形态异常所必需的，但不是microRNA途径中相关缺陷所必需的。全基因组镶嵌微阵列实验表明，已知沉默所需的基因的表达在HC-Pro植物中是不变的，而参与其他生物和非生物胁迫反应的基因的数量惊人的诱导，许多在RAV 2依赖的方式。在需要RAV 2来通过HC-Pro诱导的基因中，有FRY 1和CML 38，这些基因被认为是沉默的内源性抑制因子。这些发现提出了一种有趣的可能性，即HC-Pro抑制沉默不是由沉默所需的基因表达减少引起的，而是由诱导应激和防御反应引起的，其中一些组分干扰抗病毒沉默。此外，两个不相关的病毒抑制因子需要相同因子的活性来阻断沉默的观察结果表明，RAV 2代表了可以容易地被病毒破坏以阻断抗病毒沉默的控制点。RNA沉默是植物中重要的抗病毒防御，许多植物病毒编码阻断RNA沉默的蛋白。然而，病毒抑制剂的作用机制是复杂的，并且对宿主植物蛋白在该过程中的作用知之甚少。在这里，我们报告的第一个例子的宿主蛋白质，发挥了所需的作用，在病毒抑制沉默的转录因子称为RAV 2，是所需的抑制沉默的两个不同的和无关的病毒蛋白。对植物基因表达模式的分析表明，RAV 2是诱导参与其他胁迫和防御途径的许多基因所必需的，包括涉及植物沉默抑制因子的基因。总体而言，结果表明，RAV 2是病毒抑制沉默的重要因素，RAV 2的作用是将宿主防御转向干扰抗病毒沉默的反应。
RNA silencing is a highly conserved pathway in the network of interconnected defense responses that are activated during viral infection. As a counter-defense, many plant viruses encode proteins that block silencing, often also interfering with endogenous small RNA pathways. However, the mechanism of action of viral suppressors is not well understood and the role of host factors in the process is just beginning to emerge. Here we report that the ethylene-inducible transcription factor RAV2 is required for suppression of RNA silencing by two unrelated plant viral proteins, potyvirus HC-Pro and carmovirus P38. Using a hairpin transgene silencing system, we find that both viral suppressors require RAV2 to block the activity of primary siRNAs, whereas suppression of transitive silencing is RAV2-independent. RAV2 is also required for many HC-Pro-mediated morphological anomalies in transgenic plants, but not for the associated defects in the microRNA pathway. Whole genome tiling microarray experiments demonstrate that expression of genes known to be required for silencing is unchanged in HC-Pro plants, whereas a striking number of genes involved in other biotic and abiotic stress responses are induced, many in a RAV2-dependent manner. Among the genes that require RAV2 for induction by HC-Pro are FRY1 and CML38, genes implicated as endogenous suppressors of silencing. These findings raise the intriguing possibility that HC-Pro-suppression of silencing is not caused by decreased expression of genes that are required for silencing, but instead, by induction of stress and defense responses, some components of which interfere with antiviral silencing. Furthermore, the observation that two unrelated viral suppressors require the activity of the same factor to block silencing suggests that RAV2 represents a control point that can be readily subverted by viruses to block antiviral silencing. RNA silencing is an important antiviral defense in plants, and many plant viruses encode proteins that block RNA silencing. However, the mechanism of action of the viral suppressors is complex, and little is known about the role of host plant proteins in the process. Here we report the first example of a host protein that plays a required role in viral suppression of silencing—a transcription factor called RAV2 that is required for suppression of silencing by two different and unrelated viral proteins. Analysis of plant gene expression patterns shows that RAV2 is required for induction of many genes involved in other stress and defense pathways, including genes implicated as plant suppressors of silencing. Overall, the results suggest that RAV2 is an important factor in viral suppression of silencing and that the role of RAV2 is to divert host defenses toward responses that interfere with antiviral silencing.
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DOI：
10.1073/pnas.95.22.13079
发表时间：
1998-10-27
影响因子：
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作者：
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通讯作者：
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