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多瘤病毒VP1的突变允许其在未分化细胞中进行体外生长，并改变体内组织复制特异性。

Mutations of polyomavirus VP1 allow in vitro growth in undifferentiated cells and modify in vivo tissue replication specificity.

作者信息

Mezes B, Amati P

机构信息

Istituto Pasteur-Fondazione Cenci Bolognetti, Dipartimento di Biopatologia Umana, Policlinico Umberto I, Università di Roma La Sapienza, Italy.

出版信息

J Virol. 1994 Feb;68(2):1196-9. doi: 10.1128/JVI.68.2.1196-1199.1994.

DOI:10.1128/JVI.68.2.1196-1199.1994
PMID:8289350
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC236560/
Abstract

Mutants of polyomavirus with altered host specificities were isolated in undifferentiated C2 myoblast cells (L. Ricci, R. Maione, C. Passananti, A. Felsani, and P. Amati, J. Virol. 66:7153-7158, 1992). The mutations responsible for this phenotype belonged to either of the two classes: a large duplication of the enhancer region or a 6-bp deletion in the VP1 coding region. Since both classes of mutations enabled the virus to grow in undifferentiated myoblast cells, we investigated their ability to replicate in embryonal carcinoma cells and in various tissues in newborn mice. Our results show that both kinds of mutations confer the ability to replicate in vitro in embryonal carcinoma F9 cells; the VP1 mutants acquired an in vivo host range of replication which is different from that of their original wild-type strain, whereas the mutation in the regulatory region did not alter the in vivo growth spectrum.

摘要

在未分化的C2成肌细胞中分离出了宿主特异性发生改变的多瘤病毒突变体（L. 里奇、R. 马奥内、C. 帕萨南蒂、A. 费尔萨尼和P. 阿马蒂，《病毒学杂志》66:7153 - 7158，1992年）。导致这种表型的突变属于以下两类中的任何一类：增强子区域的大片段重复或VP1编码区域的6个碱基对缺失。由于这两类突变都使病毒能够在未分化的成肌细胞中生长，我们研究了它们在胚胎癌细胞和新生小鼠各种组织中的复制能力。我们的结果表明，这两种突变都赋予了在体外胚胎癌F9细胞中复制的能力；VP1突变体获得了与原始野生型菌株不同的体内宿主复制范围，而调节区域的突变并未改变体内生长谱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/236560/3b5bf2f1f574/jvirol00011-0630-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/236560/2893fd12a5e0/jvirol00011-0629-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/236560/b0dea3b384be/jvirol00011-0629-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/236560/3b5bf2f1f574/jvirol00011-0630-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/236560/2893fd12a5e0/jvirol00011-0629-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/236560/b0dea3b384be/jvirol00011-0629-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/236560/3b5bf2f1f574/jvirol00011-0630-a.jpg

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本文引用的文献

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The transactivator proteins VP16 and GAL4 bind replication factor A.反式激活蛋白VP16和GAL4与复制因子A结合。
Cell. 1993 Jun 18;73(6):1223-32. doi: 10.1016/0092-8674(93)90650-f.
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Detection of DNA and RNA virus genomes in organ systems of whole mice: patterns of mouse organ infection by polyomavirus.全小鼠器官系统中DNA和RNA病毒基因组的检测：多瘤病毒对小鼠器官的感染模式
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负责诱导α基因的单纯疱疹病毒粒子相关因子的特性分析
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Polyoma DNA sequences involved in control of viral gene expression in murine embryonal carcinoma cells.参与小鼠胚胎癌细胞中病毒基因表达调控的多瘤病毒DNA序列。
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Identification of herpes simplex virus DNA sequences which encode a trans-acting polypeptide responsible for stimulation of immediate early transcription.鉴定编码负责刺激即刻早期转录的反式作用多肽的单纯疱疹病毒DNA序列。
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