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Activation of polyomavirus DNA replication by yeast GAL4 is dependent on its transcriptional activation domains.

作者信息

Bennett-Cook E R, Hassell J A

机构信息

Institute for Molecular Biology and Biotechnology, McMaster University, Hamilton, Ontario, Canada.

出版信息

EMBO J. 1991 Apr;10(4):959-69. doi: 10.1002/j.1460-2075.1991.tb08030.x.

DOI:10.1002/j.1460-2075.1991.tb08030.x
PMID:1849079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC452740/
Abstract

The polyomavirus replication origin contains transcriptional regulatory sequences. To determine how these elements function in DNA replication, and to learn whether a common mechanism underlies the activation of transcription and DNA replication, we tested whether a well-characterized transcriptional activator, yeast GAL4, was capable of stimulating DNA replication and transcription in the same mammalian cell line. We observed that GAL4 activated polyomavirus DNA replication in mouse cells when its binding site was juxtaposed to the late border of the polyomavirus origin core. Synergistic activation of DNA replication was achieved by multimerization of the GAL4 binding site. Analysis of GAL4 mutant proteins, GAL4 hybrid proteins and mutants of the latter revealed that the activation domains of these transcriptional activators were required to stimulate DNA replication. In agreement with previously published data, the activation domains of GAL4 were also required to enhance transcription in the same mouse cell line. These observations implicate transcriptional activators in Py DNA replication and suggest that similar mechanisms govern the activation of transcription and DNA replication.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a911/452740/50c79da0959c/emboj00102-0231-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a911/452740/117f7d864948/emboj00102-0226-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a911/452740/92c97b051b80/emboj00102-0227-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a911/452740/f81a0eb2f842/emboj00102-0229-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a911/452740/d4444f2b2679/emboj00102-0230-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a911/452740/50c79da0959c/emboj00102-0231-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a911/452740/117f7d864948/emboj00102-0226-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a911/452740/92c97b051b80/emboj00102-0227-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a911/452740/f81a0eb2f842/emboj00102-0229-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a911/452740/d4444f2b2679/emboj00102-0230-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a911/452740/50c79da0959c/emboj00102-0231-a.jpg

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引用本文的文献

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Stimulation of DNA replication from the polyomavirus origin by PCAF and GCN5 acetyltransferases: acetylation of large T antigen.

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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Saccharomyces cerevisiae GAL1-GAL10 divergent promoter region: location and function of the upstream activating sequence UASG.酿酒酵母GAL1 - GAL10双向启动子区域:上游激活序列UASG的定位与功能
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Use of lacZ fusions to delimit regulatory elements of the inducible divergent GAL1-GAL10 promoter in Saccharomyces cerevisiae.
PCAF和GCN5乙酰转移酶对多瘤病毒起源的DNA复制的刺激作用:大T抗原的乙酰化
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The capacity of polyomavirus enhancer binding protein 2alphaB (AML1/Cbfa2) to stimulate polyomavirus DNA replication is related to its affinity for the nuclear matrix.多瘤病毒增强子结合蛋白2αB(AML1/Cbfa2)刺激多瘤病毒DNA复制的能力与其对核基质的亲和力有关。
Mol Cell Biol. 1998 Jul;18(7):4165-76. doi: 10.1128/MCB.18.7.4165.
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cis elements that contribute to geminivirus transcriptional regulation and the efficiency of DNA replication.有助于双生病毒转录调控和DNA复制效率的顺式元件。
J Virol. 1997 Sep;71(9):6947-55. doi: 10.1128/JVI.71.9.6947-6955.1997.
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Functional interactions between papillomavirus E1 and E2 proteins.乳头瘤病毒E1和E2蛋白之间的功能相互作用。
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c-Jun stimulates origin-dependent DNA unwinding by polyomavirus large Tantigen.c-Jun通过多瘤病毒大T抗原刺激依赖于起始点的DNA解旋。
EMBO J. 1996 Oct 15;15(20):5636-46.
8
Transcriptional activation function is not required for stimulation of DNA replication by bovine papillomavirus type 1 E2.1型牛乳头瘤病毒E2刺激DNA复制并不需要转录激活功能。
J Virol. 1996 Oct;70(10):7264-9. doi: 10.1128/JVI.70.10.7264-7269.1996.
9
Co-operative interaction between the initiator E1 and the transcriptional activator E2 is required for replicator specific DNA replication of bovine papillomavirus in vivo and in vitro.引发因子E1与转录激活因子E2之间的协同相互作用是牛乳头瘤病毒在体内和体外进行复制子特异性DNA复制所必需的。
EMBO J. 1995 Dec 15;14(24):6218-28. doi: 10.1002/j.1460-2075.1995.tb00312.x.
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p53 inhibits DNA replication in vitro in a DNA-binding-dependent manner.p53在体外以DNA结合依赖的方式抑制DNA复制。
Mol Cell Biol. 1995 Dec;15(12):6554-60. doi: 10.1128/MCB.15.12.6554.
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Mol Cell Biol. 1984 Oct;4(10):1985-98. doi: 10.1128/mcb.4.10.1985-1998.1984.
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Polyomavirus origin for DNA replication comprises multiple genetic elements.多瘤病毒DNA复制的起源包含多个遗传元件。
J Virol. 1983 Sep;47(3):586-99. doi: 10.1128/JVI.47.3.586-599.1983.
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Territorial limits and functional anatomy of the simian virus 40 replication origin.猿猴病毒40复制起点的区域界限和功能解剖结构。
Proc Natl Acad Sci U S A. 1982 Jan;79(2):381-5. doi: 10.1073/pnas.79.2.381.
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Polyoma mutants that productively infect F9 embryonal carcinoma cells do not rescue wild-type polyoma in F9 cells.能有效感染F9胚胎癌细胞的多瘤病毒突变体无法拯救F9细胞中的野生型多瘤病毒。
Proc Natl Acad Sci U S A. 1982 Mar;79(5):1479-83. doi: 10.1073/pnas.79.5.1479.
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。
Nucleic Acids Res. 1981 Dec 11;9(23):6231-50. doi: 10.1093/nar/9.23.6231.
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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。
Nature. 1981 Sep 3;293(5827):79-81. doi: 10.1038/293079a0.
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Mutation near the polyoma DNA replication origin permits productive infection of F9 embryonal carcinoma cells.多瘤病毒DNA复制起点附近的突变允许F9胚胎癌细胞进行有效感染。
Cell. 1981 Mar;23(3):809-14. doi: 10.1016/0092-8674(81)90445-1.
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Isolation of mutants of an animal virus in bacteria.在细菌中分离动物病毒的突变体。
Science. 1980 Sep 19;209(4463):1392-6. doi: 10.1126/science.6251547.