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Loss of DNA-binding and new transcriptional trans-activation function in polyomavirus large T-antigen with mutation of zinc finger motif.

作者信息

Bergqvist A, Nilsson M, Bondeson K, Magnusson G

机构信息

Department of Medical Virology, Uppsala University Biomedical Center, Sweden.

出版信息

Nucleic Acids Res. 1990 May 11;18(9):2715-20. doi: 10.1093/nar/18.9.2715.

DOI:10.1093/nar/18.9.2715
PMID:2160069
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC330756/
Abstract

A putative zinc finger in polyomavirus large T-antigen was investigated. We were unable to demonstrate unequivocally a requirement for zinc in specific DNA-binding using the chelating agent 1, 10-phenanthroline. An involvement of the putative zinc finger in specific DNA-binding was nevertheless suggested by the properties of a mutant protein with a cys----ser replacement in the finger motif. Probably as a result of the defective DNA-binding, the mutant protein had lost its activity in initiation of viral DNA-replication and in negative regulation of viral early transcription. However, the trans-activation of the viral late promoter was normal. The analysis also revealed a previously unrecognized activity of large T-antigen. The mutant protein trans-activated the viral early promoter. In the wild-type protein this activity is probably concealed by the separate, negative regulatory function.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a80a/330756/34190498b194/nar00193-0134-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a80a/330756/66446b0a98a9/nar00193-0132-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a80a/330756/05607c1403d9/nar00193-0133-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a80a/330756/d05aeba1b9c2/nar00193-0133-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a80a/330756/34190498b194/nar00193-0134-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a80a/330756/66446b0a98a9/nar00193-0132-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a80a/330756/05607c1403d9/nar00193-0133-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a80a/330756/d05aeba1b9c2/nar00193-0133-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a80a/330756/34190498b194/nar00193-0134-a.jpg

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引用本文的文献

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本文引用的文献

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Recombinant genomes which express chloramphenicol acetyltransferase in mammalian cells.在哺乳动物细胞中表达氯霉素乙酰转移酶的重组基因组。
Mol Cell Biol. 1982 Sep;2(9):1044-51. doi: 10.1128/mcb.2.9.1044-1051.1982.
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T-antigen expression by polyoma mutants with modified RNA splicing.
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多瘤病毒大T抗原锌指介导的锌结合和蛋白质-蛋白质相互作用。
J Virol. 1995 May;69(5):2842-9. doi: 10.1128/JVI.69.5.2842-2849.1995.
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The DNA-binding properties of polyomavirus large T antigen are altered by ATP and other nucleotides.多瘤病毒大T抗原的DNA结合特性会因ATP和其他核苷酸而改变。
J Virol. 1991 Feb;65(2):687-99. doi: 10.1128/JVI.65.2.687-699.1991.
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Determination of the origin-specific DNA-binding domain of polyomavirus large T antigen.多瘤病毒大T抗原的起源特异性DNA结合结构域的测定。
J Virol. 1991 Dec;65(12):6998-7003. doi: 10.1128/JVI.65.12.6998-7003.1991.
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Oncogenes result in genomic alterations that activate a transcriptionally silent, dominantly selectable reporter gene (neo).致癌基因会导致基因组改变，从而激活一个转录沉默的、具有显性选择标记的报告基因（新霉素抗性基因）。
Mol Cell Biol. 1992 Jan;12(1):198-206. doi: 10.1128/mcb.12.1.198-206.1992.
Cell. 1984 Feb;36(2):381-9. doi: 10.1016/0092-8674(84)90231-9.
4
Polyomavirus large T antigen binds independently to multiple, unique regions on the viral genome.多瘤病毒大T抗原独立地与病毒基因组上多个独特区域结合。
J Virol. 1983 Sep;47(3):600-10. doi: 10.1128/JVI.47.3.600-610.1983.
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High efficiency polyoma DNA transfection of chloroquine treated cells.氯喹处理细胞的高效多瘤病毒DNA转染
Nucleic Acids Res. 1983 Mar 11;11(5):1295-308. doi: 10.1093/nar/11.5.1295.
6
Deletions of N-terminal sequences of polyoma virus T-antigens reduce but do not abolish transformation of rat fibroblasts.多瘤病毒T抗原N端序列的缺失会降低但不会消除大鼠成纤维细胞的转化。
Mol Cell Biol. 1982 Oct;2(10):1238-46. doi: 10.1128/mcb.2.10.1238-1246.1982.
7
A region of the polyoma virus genome between the replication origin and late protein coding sequences is required in cis for both early gene expression and viral DNA replication.多瘤病毒基因组中位于复制起点和晚期蛋白编码序列之间的区域对于早期基因表达和病毒DNA复制而言，在顺式作用中是必需的。
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Inhibition of SV40 replication in simian cells by specific pBR322 DNA sequences.特定pBR322 DNA序列对猴细胞中SV40复制的抑制作用。
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Binding of a simian virus 40 T antigen-related protein to DNA.一种猿猴病毒40 T抗原相关蛋白与DNA的结合。
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Regulation of simian virus 40 early transcription in vitro by a purified tumor antigen.一种纯化的肿瘤抗原对猿猴病毒40早期转录的体外调控
Proc Natl Acad Sci U S A. 1980 Oct;77(10):5706-10. doi: 10.1073/pnas.77.10.5706.