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对一株从美人蕉上分离到的CMV(Cah1-CMV)进行了全长克隆、全序列分析及寄主生物学研究。结果显示:其RNA1全长为3 356 nt,编码993个aa的1a蛋白;RNA2全长为3 045 nt,编码843 aa的2a蛋白和111 aa的2b蛋白;RNA3全长为2 220 nt,编码279 aa的3a蛋白和218 aa的CP蛋白。系统进化树分析显示:Cah1-CMV是CMV亚组IB株系。但是,该株系可以通过汁液摩擦接种侵染烟草(Nicotiana tabacum)、心叶烟(N.glutinosa)和番茄(Lycopersivon esculentum)鉴别寄主,可引起心叶烟顶端坏死,而在其他茄科寄主上均为典型花叶。将Cah1-CMV的2b替换到Fny-CMV中,产生FCah12b-CMV重组体,分析其在心叶烟上的致病性。结果显示:侵染早期,FCah12b-CMV引起心叶烟顶端叶黄褐坏死,与其母本病毒Cah1-CMV的症状相似,而非Fny-CMV症状;侵染后期,FCah12b-CMV并不引起植株系统性坏死。Northern blot-ting结果显示:Cah1-CMV、FCah12b-CMV和Fny-CMV在系统叶中的积累水平不存在明显差异。以上结果说明Cah1-CMV的2b基因在Cah1-CMV致病过程中具有重要功能,但并不是整株症状的决定因子;致病性差异与其基因组RNA在寄主体内的积累水平并不呈正相关性。
A full-length cloning, full sequence analysis and host biology study of CMV (Cah1-CMV) isolated from canna was conducted. The results showed that the total length of RNA1 was 3 356 nt, which encoded 993 aa of 1a protein. RNA2 full length was 3 045 nt, encoding 843 aa of 2a protein and 111 aa of 2b protein. 279 aa of the 3a protein and 218 aa of the CP protein. Phylogenetic tree analysis showed that Cah1-CMV is a CMV subgroup IB strain. However, this strain can identify the host of Nicotiana tabacum, N. glutinosa and Lycopersivon esculentum through frictional inoculation of the juice, which can cause the apical necrosis of leaf discs, whereas on other solanaceous hosts Are typical mosaic. Substitution of 2b of Cah1-CMV into Fny-CMV resulted in a recombinant FCah12b-CMV that was assayed for pathogenicity on leaflet smoke. The results showed that FCah12b-CMV caused the yellow-brown necrosis on the apical leaf of tobacco leaf at the early stage of infection, similar to the symptoms of Cah1-CMV, but not Fny-CMV. In the late stage of infection, FCah12b-CMV did not cause plant system Necrosis. Northern blot-ting results showed that there was no significant difference in the accumulation level of Cah1-CMV, FCah12b-CMV and Fny-CMV in systemic leaves. The above results indicated that the 2b gene of Cah1-CMV plays an important role in Cah1-CMV pathogenicity, but it is not the determinant of the whole plant symptom. The pathogenicity difference is not positively correlated with the level of its genomic RNA in the host.