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多瘤病毒转化的大鼠细胞中病毒DNA的状态。I. 病毒拯救及非整合病毒DNA分子的存在

State of the viral DNA in rat cells transformed by polyoma virus. I. Virus rescue and the presence of nonintergrated viral DNA molecules.

作者信息

Prasad I, Zouzias D, Basilico C

出版信息

J Virol. 1976 May;18(2):436-44. doi: 10.1128/JVI.18.2.436-444.1976.

DOI:10.1128/JVI.18.2.436-444.1976
PMID:178887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC515568/
Abstract

The interaction of polyoma virus with a continuous line of rat cells was studied. Infection of these cells with polyoma did not cause virus multiplication but induced transformation. Transformed cells did not produce infectious virus, but in all clones tested virus was rescuable upon fusion with permissive mouse cells. Transformed rat cells contained, in addition to integrated viral genomes, 20 to 50 copies of nonintegrated viral DNA equivalents per cell (average). "Free" viral DNA molecules were also found in cells transformed by the ts-a and ts-8 polyoma mutants and kept at 33 C. This was not due to a virus carrier state, since the number of nonintegrated viral DNA molecules was found to be unchanged when cells were grown in the presence of antipolyoma serum. Recloning of the transformed cell lines produced subclones, which also contained free viral DNA. Most of these molecules were supercoiled and were found in the muclei of the transformed cells. The nonintegrated viral DNA is infectious. Its specifici infectivity is, however, about 100-fold lower than that of polyoma DNA extracted from productively infected cells, suggesting that these molecules contain a large proportion of defectives.

摘要

研究了多瘤病毒与大鼠细胞连续系的相互作用。用多瘤病毒感染这些细胞不会导致病毒增殖,但会诱导细胞转化。转化后的细胞不产生感染性病毒,但在所有测试的克隆中,与允许性小鼠细胞融合后病毒均可被拯救。除整合的病毒基因组外,转化后的大鼠细胞每个细胞平均还含有20至50个非整合病毒DNA等效拷贝。在由ts-a和ts-8多瘤病毒突变体转化并保持在33℃的细胞中也发现了“游离”病毒DNA分子。这并非由于病毒携带状态,因为当细胞在抗多瘤病毒血清存在下生长时,发现非整合病毒DNA分子的数量没有变化。对转化细胞系进行再克隆产生了亚克隆,这些亚克隆也含有游离病毒DNA。这些分子大多是超螺旋的,存在于转化细胞的细胞核中。非整合病毒DNA具有感染性。然而,其比感染性比从生产性感染细胞中提取的多瘤病毒DNA低约100倍,这表明这些分子包含很大比例的缺陷型。

相似文献

1
State of the viral DNA in rat cells transformed by polyoma virus. I. Virus rescue and the presence of nonintergrated viral DNA molecules.多瘤病毒转化的大鼠细胞中病毒DNA的状态。I. 病毒拯救及非整合病毒DNA分子的存在
J Virol. 1976 May;18(2):436-44. doi: 10.1128/JVI.18.2.436-444.1976.
2
State of the viral DNA in rat cells transformed by polyma virus. II. Identification of the cells containing nonintegrated viral DNA and the effect of viral mutations.多瘤病毒转化的大鼠细胞中病毒DNA的状态。II. 含有未整合病毒DNA的细胞的鉴定及病毒突变的影响。
J Virol. 1977 Oct;24(1):142-50. doi: 10.1128/JVI.24.1.142-150.1977.
3
Induction of virus synthesis in polyoma-transformed BHK-21 cells.多瘤病毒转化的BHK - 21细胞中病毒合成的诱导。
J Virol. 1973 Mar;11(3):424-31. doi: 10.1128/JVI.11.3.424-431.1973.
4
Loss of integrated viral DNA sequences in polyomatransformed cells is associated with an active viral A function.多瘤病毒转化细胞中整合病毒DNA序列的丢失与活跃的病毒A功能相关。
Cell. 1979 Jul;17(3):645-59. doi: 10.1016/0092-8674(79)90272-1.
5
Relationship between integrated and nonintegrated viral DNA in rat cells transformed by polyoma virus.多瘤病毒转化的大鼠细胞中整合型与非整合型病毒DNA之间的关系。
J Virol. 1980 Jun;34(3):615-26. doi: 10.1128/JVI.34.3.615-626.1980.
6
Multiple free viral DNA copies in polyoma virus-transformed mouse cells surviving productive infection.在经历增殖性感染后存活的多瘤病毒转化的小鼠细胞中存在多个游离病毒DNA拷贝。
J Virol. 1977 Jun;22(3):646-53. doi: 10.1128/JVI.22.3.646-653.1977.
7
State and organization of polyoma virus DNA sequences in transformed rat cell lines.转化大鼠细胞系中多瘤病毒DNA序列的状态与组织形式
J Virol. 1979 Feb;29(2):633-48. doi: 10.1128/JVI.29.2.633-648.1979.
8
Polyoma virus-transformed rat cell lines inducible for viral capsid antigen synthesis.
Virology. 1975 Jun;65(2):446-54. doi: 10.1016/0042-6822(75)90050-1.
9
Requirements for excision and amplification of integrated viral DNA molecules in polyoma virus-transformed cells.多瘤病毒转化细胞中整合病毒DNA分子的切除和扩增要求。
J Virol. 1982 Aug;43(2):617-28. doi: 10.1128/JVI.43.2.617-628.1982.
10
Induction of virus multiplication in permissive cells transformed by a temperature-sensitive polyoma virus. I. Isolation and partial characterization of survivors.
Intervirology. 1980;14(3-4):180-9. doi: 10.1159/000149181.

引用本文的文献

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Primary rat cells expressing a hybrid polyomavirus-simian virus 40 large T antigen have altered growth properties.表达杂交多瘤病毒-猿猴病毒40大T抗原的原代大鼠细胞具有改变的生长特性。
J Virol. 1993 Aug;67(8):4750-9. doi: 10.1128/JVI.67.8.4750-4759.1993.
2
The kinetics of simian virus 40-induced progression of quiescent cells into S phase depend on four independent functions of large T antigen.猿猴病毒40诱导静止细胞进入S期的动力学取决于大T抗原的四种独立功能。
J Virol. 1994 Sep;68(9):5496-508. doi: 10.1128/JVI.68.9.5496-5508.1994.
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Degradation of endothelial cell matrix collagen is correlated with induction of stromelysin by an activated ras oncogene.内皮细胞基质胶原蛋白的降解与活化的ras癌基因诱导基质溶解素相关。
Clin Exp Metastasis. 1995 Jul;13(4):236-48. doi: 10.1007/BF00133479.
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Anemia- and polycythemia-inducing isolates of Friend spleen focus-forming virus. Biological and molecular evidence for two distinct viral genomes.弗氏脾脏灶形成病毒的贫血和红细胞增多诱导分离株。两种不同病毒基因组的生物学和分子证据。
J Exp Med. 1980 Jun 1;151(6):1477-92. doi: 10.1084/jem.151.6.1477.
5
Ca2+ and Mg2+ requirements for growth are not concomitantly reduced during cell transformation.细胞转化过程中,生长所需的Ca2+和Mg2+需求并非同时降低。
Mol Cell Biochem. 1984;59(1-2):173-81. doi: 10.1007/BF00231313.
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New rat cell line that is highly susceptible to transformation by several oncogenes.
Mol Cell Biol. 1984 Dec;4(12):2925-8. doi: 10.1128/mcb.4.12.2925-2928.1984.
7
Deletion of the origin of replication impairs the ability of polyomavirus DNA to transform cells and to form tandem insertions.复制起点的缺失会损害多瘤病毒DNA转化细胞以及形成串联插入的能力。
J Virol. 1984 Mar;49(3):984-7. doi: 10.1128/JVI.49.3.984-987.1984.
8
Papovaviral persistent infections.乳头多瘤空泡病毒持续性感染
Microbiol Rev. 1982 Dec;46(4):384-425. doi: 10.1128/mr.46.4.384-425.1982.
9
mlt Mutants of polyoma virus.多瘤病毒的mlt突变体
J Virol. 1982 Dec;44(3):1080-3. doi: 10.1128/JVI.44.3.1080-1083.1982.
10
Increased activity of polynucleotide ligase in 5-iodo-2'-deoxyuridine and mitomycin C-pretreated simian virus 40 (SV40)-infected monkey kidney cells.在经5-碘-2'-脱氧尿苷和丝裂霉素C预处理的感染猿猴病毒40(SV40)的猴肾细胞中,多核苷酸连接酶的活性增加。
Nucleic Acids Res. 1982 Aug 25;10(16):5073-84. doi: 10.1093/nar/10.16.5073.

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