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首页> 外文期刊>Molecular Plant-Microbe Interactions >Adaptation of Soybean mosaic virus Avirulent Chimeras Containing P3 Sequences from Virulent Strains to Rsv1-Genotype Soybeans Is Mediated by Mutations in HC-Pro
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Adaptation of Soybean mosaic virus Avirulent Chimeras Containing P3 Sequences from Virulent Strains to Rsv1-Genotype Soybeans Is Mediated by Mutations in HC-Pro

机译:HC-Pro中的突变介导了含有来自毒株的P3序列的毒力嵌合体从毒株到Rsv1基因型大豆的适应。

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In Rsv1 -genotype soybean, Soybean mosaic virus (SMV)-N (an avirulent isolate of strain G2) elicits extreme resistance (ER) whereas strain SMV-G7 provokes a lethal systemic hypersensitive response (LSHR). SMV-G7d, an experimentally evolved variant of SMV-G7, induces systemic mosaic. Thus, for Rsv1 -genotype soybean, SMV-N is avirulent whereas SMV-G7 and SMV-G7d are both virulent. Exploiting these differential interactions, we recently mapped the elicitor functions of SMV provoking Rsv1 -mediated ER and LSHR to the N-terminal 271 amino acids of P3 from SMV-N and SMV-G7, respectively. The phenotype of both SMV-G7 and SMV-G7d were rendered avirulent on Rsv1 -genotype soybean when the part of the genome encoding the N-terminus or the entire P3 cistron was replaced with that from SMV-N; however, reciprocal exchanges did not confer virulence to SMV-N-derived P3 chimeras. Here, we describe virulent SMV-N-derived P3 chimeras containing the full-length or the N-terminal P3 from SMV-G7 or SMV-G7d, with or without additional mutations in P3, that were selected on Rsv1 -genotype soybean by sequential transfers on rsv1 and Rsv1 -genotype soybean. Sequence analyses of the P3 and helper-component proteinase (HC-Pro) cistrons of progeny recovered from Rsv1 -genotype soybean consistently revealed the presence of mutations in HC-Pro. Interestingly, the precise mutations in HC-Pro required for the adaptation varied among the chimeras. No mutation was detected in the HC-Pro of progeny passaged continuously in rsv1 -genotype soybean, suggesting that selection is a consequence of pressure imposed by Rsv1 . Mutations in HC-Pro alone failed to confer virulence to SMV-N; however, reconstruction of mutations in HC-Pro of the SMV-N-derived P3 chimeras resulted in virulence. Taken together, the data suggest that HC-Pro complementation of P3 is essential for SMV virulence on Rsv1 -genotype soybean.
机译:在Rsv1基因型大豆中,大豆花叶病毒(SMV)-N(菌株G2的无毒分离株)引起极高的抗性(ER),而菌株SMV-G7则引起致命的系统性超敏反应(LSHR)。 SMV-G7d是SMV-G7的实验进化变体,可诱导系统性镶嵌。因此,对于Rsv1基因型大豆,SMV-N是无毒的,而SMV-G7和SMV-G7d都具有毒性。利用这些差异相互作用,我们最近将激发Rsv1介导的ER和LSHR的SMV激发子功能分别映射到SMV-N和SMV-G7的P3的N端271个氨基酸。当将编码N端的基因组部分或整个P3顺反子的基因组部分替换为SMV-N的基因时,SMV-G7和SMV-G7d的表型在Rsv1基因型大豆上变得无毒。但是,相互交换并不会赋予SMV-N衍生的P3嵌合体毒性。在这里,我们描述了强毒的SMV-N衍生的P3嵌合体,其中包含来自SMV-G7或SMV-G7d的全长或N末端P3,在P3中带有或不带有其他突变,这些突变是在Rsv1基因型大豆上按顺序选择的在rsv1和Rsv1基因型大豆上转移。从Rsv1基因型大豆中回收的子代的P3和辅助成分蛋白酶(HC-Pro)顺反子的序列分析始终显示HC-Pro中存在突变。有趣的是,适应所需的HC-Pro精确突变在嵌合体之间有所不同。在rsv1基因型大豆中连续传代的HC-Pro后代中未检测到突变,这表明选择是Rsv1施加压力的结果。仅HC-Pro中的突变无法赋予SMV-N致命性。然而,SMV-N衍生的P3嵌合体的HC-Pro突变的重建导致了毒力。两者合计,数据表明P3的HC-Pro互补对于Rsv1基因型大豆上的SMV毒力至关重要。

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