通过复制起点处的碱基对替换抑制多瘤病毒DNA合成。
Inhibition of polyoma DNA synthesis by base pair substitutions at the replication origin.
作者信息
Luthman H, Osterlund M, Magnusson G
出版信息
Nucleic Acids Res. 1984 Oct 11;12(19):7503-515. doi: 10.1093/nar/12.19.7503.
Abstract
The effect of base pair substitutions on the function of the polyoma virus origin of DNA replication was studied. The mutations were all C-G to T-A transitions, induced by bisulfite treatment of recombinant DNA molecules. The mutagenesis was directed to short single-stranded gaps in duplex DNA, or to loops in heteroduplex molecules. Modification of a 34 base pair sequence of dyad symmetry led to cis-acting inhibition of viral DNA synthesis, ranging from slight defects to total inactivation. One of the mutants was temperature sensitive. Mutants with base changes in an adjacent DNA segment, including an 18 base pair long purine-pyrimidine tract, had similar, but less severe, deficiences. In contrast to the effect of mutations in the homologous region of the simian virus 40 genome, there was no strict relationship between mutation of the putative large T-antigen-binding base sequence GPuGGC and defective viral DNA synthesis.
摘要
研究了碱基对替换对多瘤病毒DNA复制起点功能的影响。这些突变均为C-G到T-A的转换，由亚硫酸氢盐处理重组DNA分子诱导产生。诱变作用针对双链DNA中的短单链缺口或异源双链分子中的环。对具有二元对称性的34个碱基对序列的修饰导致病毒DNA合成的顺式作用抑制，范围从轻微缺陷到完全失活。其中一个突变体是温度敏感型的。在相邻DNA片段中发生碱基变化的突变体，包括一个18个碱基对长的嘌呤-嘧啶序列，具有相似但不太严重的缺陷。与猿猴病毒40基因组同源区域突变的影响相反，假定的大T抗原结合碱基序列GPuGGC的突变与有缺陷的病毒DNA合成之间没有严格的关系。
相似文献
1
Inhibition of polyoma DNA synthesis by base pair substitutions at the replication origin.通过复制起点处的碱基对替换抑制多瘤病毒DNA合成。
Nucleic Acids Res. 1984 Oct 11;12(19):7503-515. doi: 10.1093/nar/12.19.7503.
2
Non-contiguous segments of the polyoma genome required in cis for DNA replication.多瘤病毒基因组中DNA复制顺式作用所需的非连续片段。
J Mol Biol. 1982 Nov 15;161(4):533-50. doi: 10.1016/0022-2836(82)90406-5.
3
Analysis of polyomavirus enhancer-effect on DNA replication and early gene expression.
J Mol Biol. 1991 Apr 5;218(3):479-83. doi: 10.1016/0022-2836(91)90690-8.
4
Isolation and characterization of polyoma host range mutants that replicate in nullipotential embryonal carcinoma cells.在无潜能胚胎癌细胞中复制的多瘤病毒宿主范围突变体的分离与鉴定。
Proc Natl Acad Sci U S A. 1981 Feb;78(2):1100-4. doi: 10.1073/pnas.78.2.1100.
5
Similarity of nucleotide sequences around the origin of DNA replication in mouse polyoma virus and simian virus 40.小鼠多瘤病毒和猴病毒40中DNA复制起点周围核苷酸序列的相似性
Proc Natl Acad Sci U S A. 1978 Jan;75(1):162-6. doi: 10.1073/pnas.75.1.162.
6
Mutational analysis of DNA sequences affecting the replication of defective polyomavirus variant D-50.
Virus Res. 1986 Dec;6(3):273-86. doi: 10.1016/0168-1702(86)90075-4.
7
Sequences in the polyomavirus DNA regulatory region involved in viral DNA replication and early gene expression.多瘤病毒DNA调控区域中参与病毒DNA复制和早期基因表达的序列。
J Virol. 1985 Jun;54(3):739-49. doi: 10.1128/JVI.54.3.739-749.1985.
8
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.
9
Regulatory mutants of polyoma virus defective in DNA replication and the synthesis of early proteins.在DNA复制和早期蛋白质合成方面存在缺陷的多瘤病毒调节突变体。
Cell. 1980 Jun;20(2):401-9. doi: 10.1016/0092-8674(80)90626-1.
10
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.
引用本文的文献
1
Mutation of large T-antigen-binding site A, but not site B or C, eliminates stalling by RNA polymerase II in the intergenic region of polyomavirus DNA.大T抗原结合位点A发生突变，而非位点B或C，可消除多瘤病毒DNA基因间区域中RNA聚合酶II的停滞现象。
J Virol. 1993 Oct;67(10):5766-75. doi: 10.1128/JVI.67.10.5766-5775.1993.
2
Murine polyomavirus and simian virus 40 large T antigens produce different structural alterations in viral origin DNA.鼠多瘤病毒和猿猴病毒40大T抗原在病毒起源DNA中产生不同的结构改变。
J Virol. 1995 Dec;69(12):7579-85. doi: 10.1128/JVI.69.12.7579-7585.1995.
3
Guanine nucleotide contacts within viral DNA sequences bound by polyomavirus large T antigen.多瘤病毒大T抗原所结合的病毒DNA序列内的鸟嘌呤核苷酸接触点。
J Virol. 1986 Feb;57(2):505-14. doi: 10.1128/JVI.57.2.505-514.1986.
4
DNA sequence requirements for replication of polyomavirus DNA in vivo and in vitro.多瘤病毒DNA在体内和体外复制的DNA序列要求。
Mol Cell Biol. 1987 Oct;7(10):3694-704. doi: 10.1128/mcb.7.10.3694-3704.1987.
5
Mutational analysis of polyomavirus small-T-antigen functions in productive infection and in transformation.多瘤病毒小T抗原在生产性感染和转化中的功能的突变分析。
J Virol. 1989 May;63(5):2126-33. doi: 10.1128/JVI.63.5.2126-2133.1989.
6
Analysis of origin of DNA replication of human papovavirus BK.人乳头多瘤空泡病毒BK的DNA复制起源分析
J Virol. 1989 Jan;63(1):356-65. doi: 10.1128/JVI.63.1.356-365.1989.
7
Asp-286----Asn-286 in polyomavirus large T antigen relaxes the specificity of binding to the polyomavirus origin.多瘤病毒大T抗原中第286位氨基酸由天冬氨酸突变为天冬酰胺，会降低其与多瘤病毒复制起点结合的特异性。
J Virol. 1989 Jan;63(1):242-9. doi: 10.1128/JVI.63.1.242-249.1989.
8
Replication-dependent transactivation of the polyomavirus late promoter.多瘤病毒晚期启动子的复制依赖性反式激活
J Virol. 1990 Mar;64(3):992-1001. doi: 10.1128/JVI.64.3.992-1001.1990.
9
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.
本文引用的文献
1
Trans-complementable copy-number mutants of plasmid ColE1.质粒ColE1的反式可互补拷贝数突变体
Nature. 1980 Jan 10;283(5743):216-8. doi: 10.1038/283216a0.
2
Sealing of gaps in duplex DNA by T4 DNA ligase.利用T4 DNA连接酶封闭双链DNA中的缺口。
Nucleic Acids Res. 1982 Mar 11;10(5):1425-37. doi: 10.1093/nar/10.5.1425.
3
Local mutagenesis within deletion loops of DNA heteroduplexes.DNA异源双链体缺失环内的局部诱变
Proc Natl Acad Sci U S A. 1982 Dec;79(23):7214-7. doi: 10.1073/pnas.79.23.7214.
4
DNA binding activity of polyoma virus large tumor antigen.多瘤病毒大肿瘤抗原的DNA结合活性。
Proc Natl Acad Sci U S A. 1984 Apr;81(7):1941-5. doi: 10.1073/pnas.81.7.1941.
5
Simian virus 40 mutant T antigens with relaxed specificity for the nucleotide sequence at the viral DNA origin of replication.对病毒DNA复制起点处核苷酸序列特异性降低的猿猴病毒40突变T抗原。
J Virol. 1984 Feb;49(2):386-93. doi: 10.1128/JVI.49.2.386-393.1984.
6
Essential contact residues within SV40 large T antigen binding sites I and II identified by alkylation-interference.通过烷基化干扰鉴定出的SV40大T抗原结合位点I和II内的必需接触残基。
Cell. 1984 Jan;36(1):155-62. doi: 10.1016/0092-8674(84)90084-9.
7
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.
8
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.
9
Ethidium-bromide-inhibited restriction endonucleases cleave one strand of circular DNA.溴化乙锭抑制的限制性内切核酸酶可切割环状DNA的一条链。
Gene. 1982 Nov;20(1):121-5. doi: 10.1016/0378-1119(82)90093-2.
10
Non-contiguous segments of the polyoma genome required in cis for DNA replication.多瘤病毒基因组中DNA复制顺式作用所需的非连续片段。
J Mol Biol. 1982 Nov 15;161(4):533-50. doi: 10.1016/0022-2836(82)90406-5.
Zotero 插件