Anderson E J, Qui S G, Schoelz J E
Department of Plant Pathology, University of Missouri, Columbia 65211.
Virology. 1991 Apr;181(2):647-55. doi: 10.1016/0042-6822(91)90898-l.
Cauliflower mosaic virus (CaMV) strains CM1841 and W260 produced markedly different symptoms when inoculated onto turnips (Brassica campestris L. 'Just Right'). The CM1841 strain induced a mild degree of stunting of infected plants while strain W260 caused moderate to severe stunting. Although CM1841 was significantly milder than W260, it accumulated to a significantly higher concentration than W260 in systemically infected leaves. We constructed a series of hybrid viruses in order to map regions of W260 responsible for enhanced disease severity relative to CM1841 and to map regions of CM1841 responsible for higher virus accumulation. We found that the characteristic degree of stunting caused by a CaMV isolate is determined in a complex manner by viral genes that influence viral gene expression and viral genes that disrupt host metabolism. Genes I and VI influenced both virus concentration and stunting severity, suggesting that these regions affected disease severity primarily through their effect on gene expression. In addition, an interaction between genes IV and VI was observed which further indicated that stunting severity was influenced by differential accumulation of virus. In contrast, three regions of W260 influenced the stunting phenotype but had no effect, or a negative effect, on virus concentration. The three regions contained (1) portions of genes II and III, (2) gene IV, independent of gene VI, and (3) the 3' half of gene V and the 19 S promoter. These regions may influence stunting severity primarily by disrupting host metabolism. Additionally, some of the chimeric viruses induced systemic necrosis on leaves, a symptom that is not characteristic of either CM1841 or W260. The necrotic flecking symptom was caused by an interaction between a W260 DNA segment containing gene I and the 5' half of gene II and a CM1841 DNA segment containing the 3' half of gene II, gene III, and gene IV.
将花椰菜花叶病毒(CaMV)的CM1841和W260毒株接种到芜菁(芜菁甘蓝‘恰到好处’品种)上时,会产生明显不同的症状。CM1841毒株使受感染植株出现轻度矮化,而W260毒株则导致中度至重度矮化。尽管CM1841毒株的症状明显比W260毒株轻,但在系统感染的叶片中,它的积累浓度却显著高于W260。我们构建了一系列杂交病毒,以便定位W260中相对于CM1841导致疾病严重程度增强的区域,以及CM1841中导致病毒积累量更高的区域。我们发现,CaMV分离株引起的特征性矮化程度是由影响病毒基因表达的病毒基因和破坏宿主新陈代谢的病毒基因以复杂方式决定的。基因I和VI既影响病毒浓度又影响矮化严重程度,这表明这些区域主要通过对基因表达的影响来影响疾病严重程度。此外,观察到基因IV和VI之间存在相互作用,这进一步表明矮化严重程度受病毒差异积累的影响。相比之下,W260的三个区域影响矮化表型,但对病毒浓度没有影响或有负面影响。这三个区域包含:(1)基因II和III的部分区域;(2)独立于基因VI的基因IV;(3)基因V的3'端一半和19S启动子。这些区域可能主要通过破坏宿主新陈代谢来影响矮化严重程度。此外,一些嵌合病毒在叶片上诱发了系统性坏死,这一症状在CM1841或W260中均不具有特征性。坏死斑点症状是由一个包含基因I和基因II 5'端一半的W260 DNA片段与一个包含基因II 3'端一半、基因III和基因IV的CM1841 DNA片段之间的相互作用引起的。