EVIDENCE FOR SIMIAN VIRUS-40 LATE TRANSCRIPTIONAL CONTROL - MIXED INFECTIONS OF WILD-TYPE SIMIAN VIRUS-40 AND A LATE LEADER DELETION MUTANT EXHIBIT TRANS EFFECTS ON LATE VIRAL-RNA SYNTHESIS

EVIDENCE FOR SIMIAN VIRUS-40 LATE TRANSCRIPTIONAL CONTROL - MIXED INFECTIONS OF WILD-TYPE SIMIAN VIRUS-40 AND A LATE LEADER DELETION MUTANT EXHIBIT TRANS EFFECTS ON LATE VIRAL-RNA SYNTHESIS
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DOI:
10.1128/jvi.42.3.798-803.1982
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发表时间:
1982-01-01
影响因子:
5.4
通讯作者:
ALWINE, JC
ALWINE, JC
中科院分区:
医学2区
文献类型:
--
作者:
ALWINE, JC

文献摘要

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与单独感染相比,涉及野生型SV 40和活缺失突变体dl 861的相等多样性的混合感染导致非洲绿色猴肾AGMK细胞胞质中野生型衍生的晚期mRNA水平降低,并且非常低至不可检测的水平的突变体衍生的晚期mRNA。dl 861缺失从晚期前导区去除16-25个碱基对。这种缺失是混合感染效应的直接原因;用野生型序列替换缺失恢复了混合感染中晚期mRNA的正常水平。其他病毒功能,早期基因表达和复制,不受dl 861缺失。混合感染效应的进一步检查表明,来自突变体和野生型基因组的晚期mRNA的未剪接核前体的水平降低或检测不到,与细胞质结果雅阁。因此,该效应似乎发生在转录水平。证明了对晚期转录的反式作用效应,这是由于混合感染中dl 861突变体的存在而可检测到的。指出了在转录水平上对SV 40晚期基因表达施加控制的扩散因子。提出了一种SV 40晚期基因表达的正调控模型。
Mixed infections involving equal multiplicities of wild-type SV40 and viable deletion mutant dl861 resulted in decreased African green monkey kidney AGMK cell cytoplasmic levels of wild-type-derived late mRNA, and very low to undetectable levels of mutant-derived late mRNA, as compared with individual infections. The dl861 deletion removes 16-25 base pairs from the late leader region. This deletion was the direct cause of the mixed-infection effect; replacement of the deletion with wild-type sequences restored normal levels of late mRNA in mixed infections. Other viral functions, early gene expression and replication, were unaffected by the dl861 deletion. Further examination of the mixed-infection effect showed that the levels of unspliced nuclear precursors of late mRNA, derived from both the mutant and wild-type genomes, were decreased or undetectable, in accord with the cytoplasmic results. Thus, the effect appears to be occurring at the transcriptional level. A trans-acting effect on late transcription, which is detectable due to the presence of the dl861 mutant in the mixed infection, was demonstrated. A diffusible factor which exerts a control on SV40 late gene expression at the transcriptional level is indicated. A model for positive control of SV40 late gene expression is presented.