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植物病毒协同作用:马铃薯Y病毒基因组编码一种广泛的致病性增强子,可反式激活异源病毒的复制。

Plant viral synergism: the potyviral genome encodes a broad-range pathogenicity enhancer that transactivates replication of heterologous viruses.

作者信息

Pruss G, Ge X, Shi X M, Carrington J C, Bowman Vance V

机构信息

Department of Biological Sciences, University of South Carolina, Columbia 29208, USA.

出版信息

Plant Cell. 1997 Jun;9(6):859-68. doi: 10.1105/tpc.9.6.859.

Abstract

Synergistic viral diseases of higher plants are caused by the interaction of two independent viruses in the same host and are characterized by dramatic increases in symptoms and in accumulation of one of the coinfecting viruses. In potato virus X (PVX)/potyviral synergism, increased pathogenicity and accumulation of PVX are mediated by the expression of potyviral 5' proximal sequences encoding P1, the helper component proteinase (HC-Pro), and a fraction of P3. Here, we report that the same potyviral sequence (termed P1/HC-Pro) enhances the pathogenicity and accumulation of two other heterologous viruses: cucumber mosaic virus and tobacco mosaic virus. In the case of PVX-potyviral synergism, we show that the expression of the HC-Pro gene product, but not the RNA sequence itself, is sufficient to induce the increase in PVX pathogenicity and that both P1 and P3 coding sequences are dispensable for this aspect of the synergistic interaction. In protoplasts, expression of the potyviral P1/HC-Pro region prolongs the accumulation of PVX (-) strand RNA and transactivates expression of a reporter gene from a PVX subgenomic promoter. Unlike the synergistic enhancement of PVX pathogenicity, which requires only expression of HC-Pro, the enhancement of PVX (-) strand RNA accumulation in protoplasts is significantly greater when the entire P1/HC-Pro sequence is expressed. These results indicate that the potyviral P1/HC-Pro region affects a step in disease development that is common to a broad range of virus infections and suggest a mechanism involving transactivation of viral replication.

摘要

高等植物的协同病毒病是由两种独立病毒在同一宿主中的相互作用引起的,其特征是症状显著加重以及其中一种共感染病毒的积累增加。在马铃薯X病毒(PVX)/马铃薯Y病毒协同作用中,PVX致病性和积累的增加是由编码P1、辅助成分蛋白酶(HC-Pro)和部分P3的马铃薯Y病毒5'近端序列的表达介导的。在此,我们报道相同的马铃薯Y病毒序列(称为P1/HC-Pro)增强了另外两种异源病毒的致病性和积累:黄瓜花叶病毒和烟草花叶病毒。在PVX-马铃薯Y病毒协同作用的情况下,我们表明HC-Pro基因产物的表达,而非RNA序列本身,足以诱导PVX致病性的增加,并且P1和P3编码序列对于协同相互作用的这一方面是可有可无的。在原生质体中,马铃薯Y病毒P1/HC-Pro区域的表达延长了PVX(-)链RNA的积累,并从PVX亚基因组启动子反式激活报告基因的表达。与仅需要HC-Pro表达的PVX致病性的协同增强不同,当表达整个P1/HC-Pro序列时,原生质体中PVX(-)链RNA积累的增强显著更大。这些结果表明,马铃薯Y病毒P1/HC-Pro区域影响了广泛病毒感染共有的疾病发展步骤,并提示了一种涉及病毒复制反式激活的机制。

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