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多瘤病毒中间T抗原是转化所必需的。

Polyoma viral middle T-antigen is required for transformation.

作者信息

Mes A M, Hassell J A

出版信息

J Virol. 1982 May;42(2):621-9. doi: 10.1128/JVI.42.2.621-629.1982.

DOI:10.1128/JVI.42.2.621-629.1982
PMID:6283174
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC256887/
Abstract

To determine whether small or middle T-antigen (or both) of polyoma virus is required for transformation, we constructed mutants of recombinant plasmids which bear the viral oncogene and measured the capacity of these mutants to transform rat cells in culture. Insertion and deletion mutations in sequences encoding small and middle T-antigens (79.7, 81.3, and 82.9 map units) rendered the DNA incapable of causing transformation by the focus assay. Similar mutations in sequences that encoded middle but not small T-antigen (89.7, 92.1, and 96.5 map units) generally abolished the transforming activity of the DNA. However, two mutants (pPdl1-4 and PPd12-7) that carried deletions at 92.1 map units retained the capacity to transform cells; pPdl1-4 did so at frequencies equal to those of the parental plasmid, whereas pPdl2-7 transformed at 10% the frequency of its antecedent. From these studies we conclude that small T-antigen alone is insufficient to cause transformation and that middle T-antigen is required for transformation, either in combination with small T-antigen or by itself.

摘要

为了确定多瘤病毒的小T抗原或中T抗原(或两者)是否是转化所必需的,我们构建了携带病毒癌基因的重组质粒突变体,并检测了这些突变体在培养物中转化大鼠细胞的能力。编码小T抗原和中T抗原(79.7、81.3和82.9图谱单位)的序列中的插入和缺失突变使DNA无法通过焦点试验导致转化。编码中T抗原但不编码小T抗原(89.7、92.1和96.5图谱单位)的序列中的类似突变通常会消除DNA的转化活性。然而,两个在92.1图谱单位处携带缺失的突变体(pPdl1-4和PPd12-7)保留了转化细胞的能力;pPdl1-4的转化频率与亲本质粒相同,而pPdl2-7的转化频率是其前身的10%。从这些研究中我们得出结论,单独的小T抗原不足以导致转化,中T抗原对于转化是必需的,要么与小T抗原联合,要么单独起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a36c/256887/468737bd2640/jvirol00158-0282-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a36c/256887/544d102fcdce/jvirol00158-0280-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a36c/256887/124d27fdf59f/jvirol00158-0281-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a36c/256887/468737bd2640/jvirol00158-0282-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a36c/256887/544d102fcdce/jvirol00158-0280-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a36c/256887/124d27fdf59f/jvirol00158-0281-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a36c/256887/468737bd2640/jvirol00158-0282-a.jpg

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本文引用的文献

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Proc Natl Acad Sci U S A. 1980 Jul;77(7):3978-82. doi: 10.1073/pnas.77.7.3978.
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Comparison of polyoma virus transcription in productively infected mouse cells and transformed rodent cell lines.多瘤病毒在产生性感染的小鼠细胞和转化的啮齿动物细胞系中的转录比较。
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Coding capacity of a 35 percent fragment of the polyoma virus genome is sufficient to initiate and maintain cellular transformation.多瘤病毒基因组35%片段的编码能力足以启动并维持细胞转化。
Proc Natl Acad Sci U S A. 1980 Jun;77(6):3278-82. doi: 10.1073/pnas.77.6.3278.
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Viable deletion mutant in the medium and large T-antigen-coding sequences of the polyoma virus genome.多瘤病毒基因组中中等大小T抗原编码序列的活缺失突变体。
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