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非允许性小鼠细胞表达猿猴病毒40晚期功能的能力。

Ability of nonpermissive mouse cells to express a simian virus 40 late function(s).

作者信息

Lange M, May E, May P

出版信息

J Virol. 1981 Jun;38(3):940-51. doi: 10.1128/JVI.38.3.940-951.1981.

DOI:10.1128/JVI.38.3.940-951.1981
PMID:6264164
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC171232/
Abstract

Mouse cells are fully nonpermissive for simian virus 40 (SV40). Infection does not lead to detectable virus replication. In this report, it was shown, first, that spliced 16S and 19S SV40 late mRNA were present in cytoplasmic and polysomal polyadenylated acid+ RNA preparations from SV40-infected baby mouse kidney cells. The 16S and 19S SV40 late mRNA's produced in infected baby mouse kidney cells were identical to or similar to the 16S and 19S SV40 late mRNA's produced in permissive monkey cells as judged by their S1 mapping patterns performed with the late strand of HpaII-BamHI fragment B and by their sedimentation patterns in a sucrose gradient. It was also shown that the 16S late mRNA from infected baby mouse kidney cells could be translated into a polypeptide which was identical to or similar to virion protein VP1 in every aspect examined, including the patter of peptide mapping by limited proteolysis. Second, we reported that mouse kidney cells produced detectable, although low, levels of SV40 virion protein VP1, as shown by the sodium dodecyl sulfate-polyacrylamide gel autoradiogram of [35S]methionine-labeled proteins immunoprecipitated by a rabbit antiserum directed against SV40 virion proteins. Third, it was reported that infected baby mouse kidney cells produced late mRNA's either (i) when the infection was done at a restrictive temperature with the nonleaky tsA58 mutant or (ii) in cells treated with 100 microgram of cycloheximide per ml, in which large T antigen synthesis was inhibited by more than 99.9%. This suggested that large T antigen was not required for the synthesis of late mRNA in mouse cells.

摘要

小鼠细胞对猿猴病毒40(SV40)完全不敏感。感染不会导致可检测到的病毒复制。在本报告中,首先表明,在感染SV40的幼鼠肾细胞的细胞质和多聚核糖体多聚腺苷酸化酸+RNA制剂中存在剪接的16S和19S SV40晚期mRNA。通过用HpaII-BamHI片段B的晚期链进行的S1图谱分析及其在蔗糖梯度中的沉降图谱判断,感染的幼鼠肾细胞中产生的16S和19S SV40晚期mRNA与允许性猴细胞中产生的16S和19S SV40晚期mRNA相同或相似。还表明,感染的幼鼠肾细胞中的16S晚期mRNA可以翻译成一种多肽,该多肽在包括有限蛋白酶解的肽图谱模式在内的各个检测方面都与病毒体蛋白VP1相同或相似。其次,我们报道,如用针对SV40病毒体蛋白的兔抗血清免疫沉淀的[35S]甲硫氨酸标记蛋白的十二烷基硫酸钠-聚丙烯酰胺凝胶放射自显影所示,小鼠肾细胞产生了可检测到的(尽管水平较低)SV40病毒体蛋白VP1。第三,据报道,感染的幼鼠肾细胞在以下情况下产生晚期mRNA:(i)用非渗漏性tsA58突变体在限制温度下进行感染时,或(ii)在每毫升用100微克环己酰亚胺处理的细胞中,其中大T抗原的合成被抑制超过99.9%。这表明在小鼠细胞中晚期mRNA的合成不需要大T抗原。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4374/171232/5acadded42f4/jvirol00006-0152-b.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4374/171232/154b59d934e1/jvirol00006-0147-a.jpg
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Metabolism of mRNA from the transforming region of adenovirus 2.腺病毒2型转化区mRNA的代谢
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