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首页> 外文期刊>Journal of Virology >Enhanced Mutability Associated with a Temperature-Sensitive Mutant of Vesicular Stomatitis Virus
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Enhanced Mutability Associated with a Temperature-Sensitive Mutant of Vesicular Stomatitis Virus

机译：增强了与温度敏感突变体的温度敏感突变体的可变性增强

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Temperature-sensitive (ts) mutant tsD1 of vesicular stomatitis virus, New Jersey serotype, is the sole representative of complementation group D. Clones derived from this mutant exhibited three different phenotypes with respect to electrophoretic mobility of the G and N polypeptides of the virion in sodium dodecyl sulfate-polyacrylamide gel. Analysis of non-ts pseudorevertants showed that none of the three phenotypes was associated with the temperature sensitivity of mutant tsD1. Additional phenotypes, some also involving the NS polypeptide, appeared during sequential cloning, indicating that mutations were generated at high frequency during replication of tsD1. Furthermore, mutations altering the electrophoretic mobility of the G, N, NS, and M polypeptides were induced in heterologous viruses multiplying in the same cells as tsD1. These heterologous viruses included another complementing ts mutant of vesicular stomatitis virus New Jersey and ts mutants of vesicular stomatitis virus Indiana and Chandipura virus. Complete or incomplete virions of tsD1 appeared to be equally efficient inducers of mutations in heterologous viruses. Analysis of the progeny of a mixed infection of two complementing ts mutants of vesicular stomatitis virus New Jersey with electrophoretically distinguishable G, N, NS, and M proteins yielded no recombinants and excluded recombination as a factor in the generation of the electrophoretic mobility variants. In vitro translation of total cytoplasmic RNA from BHK cells indicated that post-translational processing was not responsible for the aberrant electrophoretic mobility of the N, NS, and M protein mutants. Aberrant glycosylation could account for three of four G protein mutants, however. Some clones of tsD1 had an N polypeptide which migrated faster in sodium dodecyl sulfate-polyacrylamide gel than did the wild type, suggesting that the polypeptide might be shorter by about 10 amino acids. Determination of the nucleotide sequence to about 200 residues from each terminus of the N gene of one of these clones, a revertant, and the wild-type parent revealed no changes compatible with synthesis of a shorter polypeptide by premature termination or late initiation of translation. The sequence data indicated, however, that the N-protein mutant and its revertant differed from the parental wild type in two of the 399 nucleotides determined. These sequencing results and the phenomenon of enhanced mutability associated with mutant tsD1 reveal that rapid and extensive evolution of the viral genome can occur during the course of normal cytolytic infection of cultured cells.
机译：温度敏感（ TS ）突变体 TS D1的叠片口腔炎病毒，新泽西型血清型是互补组D.衍生自该突变体的克隆表现出三种不同的表型关于长甲基硫酸钠 - 聚丙烯酰胺凝胶中V和N多肽的电泳迁移率。非 TS 假性维度的分析表明，这三种表型都不是突变体 TS D1的温度敏感性相关的。在顺序克隆期间出现了另外的表型，其中一些也涉及NS多肽，表明在高频期间在 TS D1的复制期间以高频率产生突变。此外，在将与 TS D1中的相同细胞中繁成的异源病毒中诱导改变G，N，NS和M多肽的电泳迁移率的突变。这些异源病毒包括另一个互补的口腔炎病毒和 Ts 突变体的蛋白质口腔炎病毒印第安纳州和新浦黎菌病毒的突变体。 TS D1的完整或不完全恶病毒粒子似乎是异源病毒中的同等有效的突变诱导剂。用电泳可区分的G，N，NS和M蛋白的叠片口腔炎病毒新泽西术的两个补充 Ts 突变体的混合感染后代的分析不会产生重组剂，并排除重组作为一代的一个因素电泳迁移率变体。来自BHK细胞的总细胞质RNA的体外翻译表明，翻译后加工不对N，NS和M蛋白突变体的异常电泳迁移率不负责任。然而，异常的糖基化可以占四个G蛋白突变体中的三种。一些 Ts D1的克隆具有N个多肽，其在十二烷基硫酸钠 - 聚丙烯酰胺凝胶中迁移得比野生型更快，表明多肽可能短约10个氨基酸。从这些克隆，回复肢体之一的 n 基因的每个末端测定核苷酸序列到约200个残留物，揭示了通过过早的较短多肽的合成兼容的变化终止或晚期发起翻译。然而，所示的序列数据是N-蛋白质突变体及其恢复剂与所确定的399个核苷酸中的两种中的父母野生型不同。这些测序结果和与突变体 Ts d1相关的增强的可变性现象表明，在培养细胞的正常细胞溶解感染过程中，可以发生病毒基因组的快速和广泛演化。

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