Yu Weichang, Murfett Jane, Schoelz James E
Department of Plant Microbiology and Pathology, University of Missouri, Columbia, Missouri 65211, USA.
Mol Plant Microbe Interact. 2003 Jan;16(1):35-42. doi: 10.1094/MPMI.2003.16.1.35.
The gene VI protein (P6) of Cauliflower mosaic virus (CaMV) functions as a virulence factor in crucifers by eliciting chlorotic symptoms in infected plants. The ability to induce chlorosis has been associated previously with P6 through gene-swapping experiments between strains and through the development of transgenic plants that express P6. The primary role that has been identified for P6 in the CaMV infection cycle is to modify the host translation machinery to facilitate the translation of the polycistronic CaMV 35S RNA. This function for P6 has been designated as the translational transactivator (TAV) function. In the present study, we have characterized an unusual variant of P6, derived from CaMV strain D4, that does not induce chlorosis upon transformation into Arabidopsis thaliana. The level of D4 P6 produced in transgenic Arabidopsis line D4-2 was comparable to the amount found in transgenic plants homozygous for W260 and CM1841 P6, two versions of P6 that induce strong chlorotic symptoms and stunting in Arabidopsis. A complementation assay proved that P6 expressed in the D4-2 line was functional, as it could support the systemic infection of a CM1841 mutant that contained a lethal frame-shift mutation within gene VI. This complementation assay allowed us to separately assess the contribution of CM1841 gene VI to symptom development versus the contribution of other CM1841 genes. Furthermore, a previous study had shown that the TAV activity of D4 P6 was comparable to that of W260 P6. That comparative analysis of TAV function, coupled with the characterization of the D4-2 transgenic line in the present paper, indicates that the TAV function of P6 may play only a minor role in the development of chlorotic symptoms.
花椰菜花叶病毒（CaMV）的基因VI蛋白（P6）通过在受感染植物中引发褪绿症状，在十字花科植物中作为一种致病因子发挥作用。此前，通过菌株间的基因交换实验以及表达P6的转基因植物的培育，已将诱导褪绿的能力与P6联系起来。在CaMV感染周期中，已确定P6的主要作用是改变宿主翻译机制，以促进多顺反子CaMV 35S RNA的翻译。P6的这一功能被指定为翻译反式激活因子（TAV）功能。在本研究中，我们鉴定了一种源自CaMV D4株系的P6异常变体，将其转化到拟南芥中不会诱导褪绿。转基因拟南芥株系D4-2中产生的D4 P6水平与在W260和CM1841 P6纯合的转基因植物中发现的量相当，W260和CM1841 P6这两个P6版本在拟南芥中会引发强烈的褪绿症状和发育迟缓。互补试验证明，在D4-2株系中表达的P6具有功能，因为它可以支持一个CM1841突变体的系统感染，该突变体在基因VI内含有致死性移码突变。这种互补试验使我们能够分别评估CM1841基因VI对症状发展的贡献与其他CM1841基因的贡献。此外，先前的一项研究表明，D4 P6的TAV活性与W260 P6相当。TAV功能的比较分析，加上本文中对D4-2转基因株系的表征，表明P6的TAV功能在褪绿症状的发展中可能只起次要作用。
