首页> 外文期刊>Journal of Virology >Differential inhibition of host protein synthesis in L cells infected with RNA - temperature-sensitive mutants of vesicular stomatitis virus.
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Differential inhibition of host protein synthesis in L cells infected with RNA - temperature-sensitive mutants of vesicular stomatitis virus.

机译:LN细胞囊肿病毒RNA温度敏感突变体的L细胞中宿主蛋白合成的差异抑制。

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The response of mouse L cells to infection with wild-type (wt) and temperature-sensitive (ts) mutants of vesicular stomatitis virus was monitored by sodium dodecyl sulfate-polyacrylamide gel electrophoresis to delineate the synthesis of host cell and viral proteins. Experiments utilized transcriptase mutants of complementation group I (ts114 and ts13), a group IV mutant (ts44) that is restricted in total RNA synthesis (RNA-1) but not in primary transcription, and a group II mutant (ts52) variably restricted in RNA synthesis (RNA +/-). L cells infected with ts mutants at permissive temperature exhibited the wt response of progressive inhibition of host cell protein synthesis accompanied by accumulation of all five viral proteins. Mutant ts44 (IV) also switched off cell protein synthesis at restrictive temperature and accumulated all five viral proteins, but with disproportionate ratios of N and G proteins. At restrictive temperature, cells infected with group I ts mutants failed to accumulate any viral protein and did not exhibit significant reduction in host cell protein synthesis. These data suggest that vesicular stomatitis virus inhibits cell protein synthesis at a stage of viral infection after transcription and possibly translation but preceding replication of progeny viral RNA.
机译:用十二烷基硫酸钠 - 聚丙烯酰胺凝胶电泳监测小鼠L细胞对野生型(WT)和温度敏感(TS)突变体感染的响应,以描绘宿主细胞和病毒蛋白的合成。实验利用互补基团I(TS114和TS13)的转录酶突变体,IV基突变体(TS44)限制在总RNA合成(RNA-1)中但不在初级转录中,并且II族突变体(TS52)可变地限制RNA合成(RNA +/-)。 L允许温度感染TS突变体的L细胞表现出宿主细胞蛋白合成的逐渐抑制的WT反应,伴随所有五种病毒蛋白的积累。突变体TS44(IV)还在限制温度下关闭细胞蛋白合成,并积累了所有五种病毒蛋白,但含有N和G蛋白的不成比例。在限制性温度下,用基团Is突变体感染的细胞未能积累任何病毒蛋白,并且在宿主细胞蛋白质合成中没有显着降低。这些数据表明,在转录后的病毒感染阶段抑制细胞蛋白质合成,并且可能翻译,但在后代病毒RNA的复制之前。

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