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劳氏肉瘤病毒RNA的末端冗余与复制起点

Terminal redundancy and the origin of replication of Rous sarcoma virus RNA.

作者信息

Coffin J M, Haseltine W A

出版信息

Proc Natl Acad Sci U S A. 1977 May;74(5):1908-12. doi: 10.1073/pnas.74.5.1908.

Abstract

In vitro synthesis of Rous sarcoma virus DNA by the virion endogenous DNA polymerase activity is initiated on a tRNAtrp primer located near the 5' end of the genome. A major product of such synthesis is a piece of DNA 101 nucleotides long (strong stop DNA) which can be isolated covalently bound to the tRNA primer. Here we show that the strong stop DNA is complementary to the extreme 5' end of the genome. We also show that the 5' and 3' termini of the Rous sarcoma virus genome, excluding the cap and the poly(A), have the identical sequence. We propose that the function of this sequence is to facilitate elongation from the 3' end of DNA chains initiated elsewhere on the virus genome.

摘要

通过病毒粒子内源性DNA聚合酶活性在体外合成劳斯肉瘤病毒DNA,该过程起始于位于基因组5'端附近的tRNAtrp引物。这种合成的一个主要产物是一段101个核苷酸长的DNA片段(强终止DNA),它可以与tRNA引物共价结合并被分离出来。在这里,我们表明强终止DNA与基因组的最末端5'端互补。我们还表明,除了帽和聚腺苷酸外,劳斯肉瘤病毒基因组的5'和3'末端具有相同的序列。我们提出,该序列的功能是促进从病毒基因组其他位置起始的DNA链的3'端延伸。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8036/431041/21b2899747df/pnas00027-0151-a.jpg

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