Sánchez F, Martínez-Herrera D, Aguilar I, Ponz F
INIA, Laboratorio de Virología Vegetal, Madrid, Spain.
Virus Res. 1998 Jun;55(2):207-19. doi: 10.1016/s0168-1702(98)00049-5.
Full-length cDNA clones of turnip mosaic virus were assembled under the control of T7 or 35S promoter. The 35S or nopaline synthase terminator signals were introduced downstream the full length cDNA controlled by 35S promoter. Both the capped in vitro transcripts from T7 controlled template, and the cDNAs from 35S controlled plasmids were infectious on Arabidopis thaliana plants according to systemically induced symptoms and to ELISA assays. The cDNAs from 35S controlled plasmids induced local lesions in Chenopodium amaranticolor and Chenopodium quinoa plants. A spontaneous silent C/T transition, giving rise to an additional SpeI restriction site, not present in the original viral RNA template, was used as a marker of the origin of infection.
芜菁花叶病毒的全长cDNA克隆在T7或35S启动子的控制下组装。35S或胭脂碱合酶终止子信号被引入到由35S启动子控制的全长cDNA下游。根据系统诱导症状和ELISA检测，来自T7控制模板的加帽体外转录本以及来自35S控制质粒的cDNA对拟南芥植物均具有感染性。来自35S控制质粒的cDNA在苋色藜和昆诺藜植物中诱导局部病斑。一个自发的沉默C/T转换产生了一个额外的SpeI限制性酶切位点，该位点在原始病毒RNA模板中不存在，被用作感染起源的标记。
