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多瘤病毒活缺失突变体的构建与分析

Construction and analysis of viable deletion mutants of polyoma virus.

作者信息

Magnusson G, Berg P

出版信息

J Virol. 1979 Nov;32(2):523-9. doi: 10.1128/JVI.32.2.523-529.1979.

DOI:10.1128/JVI.32.2.523-529.1979
PMID:228075
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC353584/
Abstract

Viable mutants of polyoma with small deletions ranging in size from 2 to 75 base pairs were obtained by infecting 3T3 cells with polyoma DNA that had been cleaved once with HaeII endonuclease or with DNase-Mn2+ digestion. The HaeII endonuclease-cleaved DNA yielded mutants with deletions at map position 72--73, whereas the mutants generated by DNase I-Mn2+ digestion had deletions either at map position 72--73 or within the map coordinates 92 and 99. Both groups of mutants appeared to grow as well as wild-type virus in 3T3 cells. The deletions at map position 72--73 did not alter the virus's ability to transform rat cells. Hence, the region just to the early side of the origin of DNA replication is not essential for vegetative growth or transformation. But the mutants with deletions in the region between map coordinates 92 and 99, a segment thought to code for polyoma large and middle T antigens (Hutchinson et al., Cell 15:65--77, 1978; Smart and Ito, Cell 15:1427--1437, 1978; Soeda et al., Cell 17:357--370, 1979), transformed rat cells at 0.2 to 0.05 the efficiency of wild-type virus.

摘要

通过用经HaeII核酸内切酶切割一次的多瘤病毒DNA或经DNA酶-Mn2 +消化的多瘤病毒DNA感染3T3细胞,获得了大小在2至75个碱基对之间的小缺失的多瘤病毒存活突变体。经HaeII核酸内切酶切割的DNA产生了在图谱位置72 - 73处有缺失的突变体,而经DNA酶I-Mn2 +消化产生的突变体在图谱位置72 - 73处或图谱坐标92和99范围内有缺失。两组突变体在3T3细胞中的生长情况似乎与野生型病毒一样好。图谱位置72 - 73处的缺失并未改变病毒转化大鼠细胞的能力。因此,DNA复制起点早期一侧的区域对于营养生长或转化并非必不可少。但是,在图谱坐标92和99之间区域有缺失的突变体(该区域被认为编码多瘤病毒大T抗原和中T抗原,Hutchinson等人,《细胞》15:65 - 77, 1978;Smart和Ito,《细胞》15:1427 - 1437, 1978;Soeda等人,《细胞》17:357 - 370, 1979),其转化大鼠细胞的效率仅为野生型病毒的0.2至0.05倍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed64/353584/6873c4eb1de2/jvirol00191-0178-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed64/353584/f492ae2b884a/jvirol00191-0177-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed64/353584/6873c4eb1de2/jvirol00191-0178-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed64/353584/f492ae2b884a/jvirol00191-0177-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed64/353584/6873c4eb1de2/jvirol00191-0178-a.jpg

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1
Construction and analysis of viable deletion mutants of polyoma virus.多瘤病毒活缺失突变体的构建与分析
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引用本文的文献

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A mouse polyomavirus-encoded microRNA targets the cellular apoptosis pathway through Smad2 inhibition.一种小鼠多瘤病毒编码的微小RNA通过抑制Smad2靶向细胞凋亡途径。
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Transformation by polyoma virus is drastically reduced by substitution of phenylalanine for tyrosine at residue 315 of middle-sized tumor antigen.通过在中等大小肿瘤抗原的315位残基处用苯丙氨酸替代酪氨酸,多瘤病毒的转化作用大幅降低。
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Construction and expression of a recombinant DNA gene encoding a polyomavirus middle-size tumor antigen with the carboxyl terminus of the vesicular stomatitis virus glycoprotein G.编码具有水泡性口炎病毒糖蛋白G羧基末端的多瘤病毒中肿瘤抗原的重组DNA基因的构建与表达。
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Polyoma DNA: a physical map.多瘤病毒DNA:物理图谱
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Effects of adrenal glucocorticoids on polyoma virus replication.肾上腺糖皮质激素对多瘤病毒复制的影响。
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Proc Natl Acad Sci U S A. 1970 Sep;67(1):394-9. doi: 10.1073/pnas.67.1.394.
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Selective extraction of polyoma DNA from infected mouse cell cultures.从受感染的小鼠细胞培养物中选择性提取多瘤病毒DNA。
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