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首页> 外文期刊>Journal of Virology >Control of protein synthesis by a temperature-sensitive mutant of reovirus 3. I. Temperature-sensitive function of ts261-b mutant.
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Control of protein synthesis by a temperature-sensitive mutant of reovirus 3. I. Temperature-sensitive function of ts261-b mutant.

机译：葡萄禽3. I的温度敏感突变体对蛋白质合成的控制。I.TS261-B突变体的温度敏感功能。

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The ability of a temperature-sensitive (ts) mutant of reovirus, ts261-b, to synthesize virus-specific RNAs and proteins during infection at the nonpermissive temperature (37 degrees C) was investigated. The relative amounts of the mutant virus-specific single-stranded (ss) RNA's and double-stranded (ds) RNA's synthesized in cells at 37 degrees C were 20 to 25% as much as those synthesized in the wild-type virus-infected cells. The 10 segments of the mutant ds RNAs and the three size classes of the ss RNAs were synthesized in the usual proportions. The methylation of the mutant viral mRNA's (ss RNAs) was not blocked at 37 degrees C in infected cells. A striking temperature-sensitive restricted function of the ts261-b mutant was expressed in the synthesis of the viral proteins. This study, which uses an in vitro protein-synthesizing system reconstituted with an endogenous polysomal fraction and a postribosomal supernatant from reovirus-infected cells, has demonstrated that the endogenous polysomes obtained from ts261-b mutant-infected cells at 37 degrees C are not active in the synthesis of the viral polypeptides of known molecular weights, and the amounts of the mutant viral polypeptides synthesized in vitro by these polysomes are 5 to 9% of those synthesized by the corresponding fraction from wild-type-infected cells. The impaired protein-synthesizing capacity of the mutant virus-specific polysomes can be restored during maintenance of the infected cells at 30 degrees C after shift-down from 37 degrees C. The in vitro synthesis of viral polypeptides of known size by the active endogenous polysomes derived from cells infected at the permissive temperature is accelerated by the addition of the postribosomal supernatant obtained from cells infected at the permissive temperature. The postribosomal supernatant from mutant-infected cells at 37 degrees C did not have a stimulatory effect, but rather, it inhibited in vitro viral protein synthesis.
机译：研究了REOVIRUS，TS261-B的温度敏感（TS）突变体在非智能温度（37℃）感染期间在感染期间合成病毒特异性RNA和蛋白质的能力。在37℃的细胞中合成的突变病毒特异性单链（SS）RNA和双链（DS）RNA的相对量为野生型病毒感染细胞中合成的4至25％ 。突变体DS RNA和SS RNA的三种尺寸类别的10个分段以通常的比例合成。突变体病毒mRNA（SS RNA）的甲基化未在感染细胞的37℃下封闭。在病毒蛋白的合成中表达了TS261-B突变体的醒目温度敏感的局部函数。该研究使用中体外蛋白质合成系统与reovirus感染的细胞重构的体外蛋白质合成系统和从reovirus感染的细胞重构的体外上清液，已经证明，在37℃下从TS261-B突变感染的细胞获得的内源性多变体不活跃在已知分子量的病毒多肽的合成中，这些多组体的体外合成的突变病毒性多肽的量是由来自野生型感染细胞的相应级分合成的5至9％。在从37摄氏度的移位后30摄氏度的30℃下，可以在30摄氏度下在30摄氏度下维持受感染的细胞的受损蛋白合成容量。通过活性内源性多源性的已知尺寸的病毒性多肽的体外合成通过添加从允许在允许温度下感染的细胞获得的脱粒剂上清液来衍生自感染在允许温度下的细胞。从37摄氏度的突变感染细胞的松染素上清液没有刺激作用，而是抑制体外病毒蛋白质合成。

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    《Journal of Virology》 |1977年第1期|共16页
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    N Ikegami;

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  • 收录信息 美国《科学引文索引》(SCI);
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