缺失外壳蛋白羧端155-158序列对TMV侵染性的影响

Effect of C-terminal Deletion of TMV CP from 155aa to 158aa on Viral Infectivity

对野生型TMV-U1的外壳蛋白羧端进行缺失突变,观察到外壳蛋白羧端序列缺失4个氨基酸(即外壳蛋白保留154个氨基酸)的TMV154TAG能较强地系统侵染烟草,并高水平表达外壳蛋白,经过二次转接新烟草植株仍保持较强的系统侵染状况,复制完整病毒粒子。结果说明外壳蛋白羧端序列4个氨基酸序列的缺失对烟草花叶病毒感染和复制无严重影响,对利用外壳蛋白羧端缺失型病毒载体表达外源多肽技术具有一定的应用价值。

By deleting the coding region from the C-terminal of TMV CP, TMV with the truncated CP coding region for the retained 154 amino acids could infect tobacco systematically,and express CP in high levels,forming intact virus particles. The results suggested that it was unnecessary for the C-terminal partial four amino acids to sustain the viral infectivity and replication. There were some role to express longer and purer foreign peptide based on defective TMV vector.