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首页> 外文期刊>Journal of Virology >Intracellular distribution of Sindbis virus membrane proteins in BHK-21 cells infected with wild-type virus and maturation-defective mutants.
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Intracellular distribution of Sindbis virus membrane proteins in BHK-21 cells infected with wild-type virus and maturation-defective mutants.

机译：SINDBIS病毒膜蛋白在感染野生型病毒和成熟缺陷突变体中的BHK-21细胞中的细胞内分布。

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The association of Sindbis virus proteins with cellular membranes during virus maturation was examined by utilizing a technique for fractionating the membranes of BHK-21 cells into three subcellular classes, which were enriched for rough endoplasmic reticulum, smooth endoplasmic reticulum, and plasma membrane. Pulse-chase experiments with wild-type (strain SVHR) virus-infected cells showed that virus envelope proteins were incorporated initially into membranes of the rough endoplasmic reticulum and subsequently migrated to the smooth and plasma membrane fractions. Large amounts of capsid protein were associated with the plasma membrane fraction even at the earliest times postpulse, and relatively little was found associated with the other membranes, suggesting a rapid and preferential association of nucleocapsids with the plasma membrane. We also examined the intracellular processing of the proteins of two temperature-sensitive Sindbis virus mutants in pulse-chase experiments at the nonpermissive temperature. Labeled virus proteins of mutant ts-20 (complementation group E) first appeared in the rough endoplasmic reticulum and were then transported to the smooth and plasma membrane fractions, as in wild-type (strain SVHR) virus-infected cells. In cells infected with ts-23 (complementation group D), the pulse-labeled virus proteins appeared initially in the rough membrane fraction and were transported to the smooth membrane fraction, but only limited amounts reached the plasma membrane. Thus, in ts-23-infected cells, the transport of the virus-encoded proteins from the smooth membranes seemed to be defective. In both ts-20- and ts-23-infected cells the envelope precursor polypeptide PE2 was not processed to E2, and no label was incorporated into free virus at the nonpermissive temperature.
机译：通过利用用于将BHK-21细胞的膜分解成三种亚细胞类的技术来研究病毒成熟期间与细胞膜的关联。富含粗糙内质网，光滑的内质网和血浆膜。脉冲追逐野生型（菌株SVHR）病毒感染细胞的实验表明，病毒包膜蛋白最初掺入粗糙内质网的膜中，随后迁移到光滑和质膜级分。即使在药物后的最早时期，也与血浆膜分数有大量的胶囊蛋白，并且发现与其他膜相关的相对较少，表明核衣壳与血浆膜的快速和优先缔合。我们还检查了在非智能温度下脉冲呼应实验中的两个温度敏感的SINDBIS病毒突变体的细胞内加工。突变体TS-20（互补基团E）的标记病毒蛋白首先出现在粗糙的内质网中，然后作为野生型（菌株SVHR）病毒感染细胞输送到光滑和质膜级分。在用TS-23感染（互补基团D）的细胞中，脉冲标记的病毒蛋白最初出现在粗膜级分中，并将其转运到平滑的膜馏分，但仅有限的量达到质膜。因此，在TS-23感染细胞中，来自光滑膜的病毒编码蛋白的运输似乎有缺陷。在TS-20和TS-23感染的细胞中，包络前体多肽PE2未加工至E2，并且在非智能温度下没有将标记物掺入游离病毒中。

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    《Journal of Virology》 |1980年第3期|共12页
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    C Erwin; D T Brown;

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  • 收录信息 美国《科学引文索引》(SCI);
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