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首页> 外文期刊>Phytopathology >Multigenic System Controlling Viral Systemic Infection Determined by the Interactions Between Cucumber mosaic virus Genes and Quantitative Trait Loci of Soybean Cultivars
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Multigenic System Controlling Viral Systemic Infection Determined by the Interactions Between Cucumber mosaic virus Genes and Quantitative Trait Loci of Soybean Cultivars

机译:黄瓜花叶病毒基因与大豆品种数量性状位点相互作用的多基因系统控制病毒性系统感染

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摘要

Soybean 'Harosoy' is resistant to Cucumber mosaic virus soybean strain C (CMV-SC) and susceptible to CMV-S strain D (CMV-SD). Using enzyme-linked immunosorbent assay and Northern hybridization, we characterized the Harosoy resistance and found that CMV-SC did not spread systemically but was restricted to the inoculated leaves in Harosoy. Harosoy resistance was not controlled by either a dominant or recessive single gene. To dissect this system controlling long-distance movement of CMV in soybean, we constructed infectious cDNA clones of CMV-SC and CMV-SD. Using these constructs and the chimeric RNAs, we demonstrated that two viral components were required for systemic infection by the virus. The region including the entire 2b gene and the 5' region of RNA3 (mainly the 5' untranslated region) together were required. By quantitative trait locus (QTL) analysis using an F sub(2) population and the F sub(3) families derived from Harosoy and susceptible 'Nemashirazu', we also showed that at least three QTLs affected systemic infection of CMV in soybean. Our study on Harosoy resistance to CMV-SC revealed an interesting mechanism, in which multiple host and viral genes coordinately controlled viral systemic infection.
机译:大豆“ Harosoy”对黄瓜花叶病毒大豆C株(CMV-SC)耐药,对CMV-S D株(CMV-SD)敏感。使用酶联免疫吸附测定和Northern杂交,我们表征了Harosoy耐药性,发现CMV-SC不会系统传播,而是局限于Harosoy中的接种叶片。优势或隐性单基因均不能控制Harosoy抗性。为了剖析控制CMV在大豆中远距离运动的系统,我们构建了CMV-SC和CMV-SD的感染性cDNA克隆。使用这些构建体和嵌合RNA,我们证明了病毒全身感染需要两个病毒成分。需要一起包含整个2b基因的区域和RNA3的5'区域(主要是5'非翻译区域)。通过使用F sub(2)种群和源自Harosoy和易感“ Nemashirazu”的F sub(3)家族的定量性状基因座(QTL)分析,我们还显示至少三个QTL影响大豆CMV的系统感染。我们对Harosoy对CMV-SC的抗性的研究揭示了一个有趣的机制,其中多个宿主和病毒基因协同控制病毒性全身感染。

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