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通过与紫外线照射的未转化细胞融合,增强从转化的哺乳动物细胞中诱导SV40复制。

Enhanced induction of SV40 replication from transformed mammalian cells by fusion with UV-irradiated untransformed cells.

作者信息

van der Lubbe J L, van Drunen C M, Hertoghs J J, Cornelis J J, Rommelaere J, van der Eb A J

出版信息

Mutat Res. 1985 Aug;151(1):1-8. doi: 10.1016/0027-5107(85)90175-7.

DOI:10.1016/0027-5107(85)90175-7
PMID:2991760
Abstract

DNA-damaging agents such as ultraviolet (UV) light are known to cause stimulation of virus replication in SV40-transformed hamster and human cells. The dose-response curves of UV-induced SV40 replication in transformed hamster cells resemble that obtained for UV-enhanced reactivation (ER) and UV-enhanced mutagenesis (EM) of SV40 or herpes viruses in mammalian cells. We have investigated whether UV-enhanced production of SV40 from transformed hamster (THK) and human (NB-E) cells belongs to the same category of conditional responses as ER and EM. To answer this question we have made use of the phenomenon that fusion of the SV40-transformed cells with monkey cells that are permissive to SV40 results in a considerable increase in the production of SV40 virus. When THK or NB-E cells were fused with UV-irradiated CV-1 cells at various times after irradiation, induction of SV40 was further increased and reached a maximum value of 2--3-fold when fusion was delayed for 24-48 h after irradiation. The kinetics of enhanced SV40 induction resembled that of ER and EM, suggesting that the UV-stimulated part of the induction represents one of the pleiotropic responses that are transiently induced in mammalian cells by DNA-damaging agents. Evidence is presented, showing that this transient effect can be induced only in cells that are permissive to SV40 replication. This suggests that the enhanced induction observed after fusion with irradiated monkey cells may be attributed to a transient increase in the activity of "permissiveness' factors. No enhanced induction was found when the THK or NB-E cells were fused with irradiated rodent cells, that are not or only slightly permissive to SV40 replication.

摘要

已知紫外线(UV)等DNA损伤剂会刺激猿猴病毒40(SV40)转化的仓鼠和人类细胞中的病毒复制。UV诱导的SV40在转化仓鼠细胞中的剂量反应曲线类似于在哺乳动物细胞中SV40或疱疹病毒的UV增强复活(ER)和UV增强诱变(EM)所获得的曲线。我们研究了来自转化仓鼠(THK)和人类(NB-E)细胞的UV增强的SV40产生是否与ER和EM属于同一类条件反应。为了回答这个问题,我们利用了SV40转化细胞与对SV40敏感的猴细胞融合会导致SV40病毒产量大幅增加这一现象。当THK或NB-E细胞在照射后的不同时间与经UV照射的CV-1细胞融合时,SV40的诱导进一步增加,当融合在照射后延迟24 - 48小时时达到最大值2 - 3倍。增强的SV40诱导动力学类似于ER和EM,这表明诱导中UV刺激的部分代表了DNA损伤剂在哺乳动物细胞中短暂诱导的多效性反应之一。有证据表明,这种短暂效应只能在对SV40复制敏感的细胞中诱导产生。这表明与经照射的猴细胞融合后观察到的增强诱导可能归因于“敏感性”因子活性的短暂增加。当THK或NB-E细胞与经照射的对SV40复制不敏感或仅略有敏感的啮齿动物细胞融合时,未发现增强诱导。

相似文献

1
Enhanced induction of SV40 replication from transformed mammalian cells by fusion with UV-irradiated untransformed cells.通过与紫外线照射的未转化细胞融合,增强从转化的哺乳动物细胞中诱导SV40复制。
Mutat Res. 1985 Aug;151(1):1-8. doi: 10.1016/0027-5107(85)90175-7.
2
Enhanced induction of SV40 replication from transformed rat cells by fusion with UV-irradiated normal and repair-deficient human fibroblasts.通过与紫外线照射的正常及修复缺陷型人成纤维细胞融合,增强转化大鼠细胞中SV40复制的诱导。
Mutat Res. 1986 Mar;165(2):47-56. doi: 10.1016/0167-8817(86)90059-3.
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Differential effect of ultraviolet light on the induction of simian virus 40 and a cellular mutator phenotype in transformed mammalian cells.
Mutat Res. 1985 Aug;151(1):9-14. doi: 10.1016/0027-5107(85)90176-9.
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Properties of permissive monkey cells transformed by UV-irradiated simian virus 40.经紫外线照射的猿猴病毒40转化的允许性猴细胞的特性。
J Virol. 1977 May;22(2):256-66. doi: 10.1128/JVI.22.2.256-266.1977.
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UV-reactivation, virus production and mutagenesis of SV40 in VU-irradiated monkey kidney cells.紫外线照射的猴肾细胞中SV40的紫外线复活、病毒产生及诱变
Mutat Res. 1980 Jun;71(1):139-46. doi: 10.1016/0027-5107(80)90014-7.
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UV Irradiation induces an activity which stimulates Simian virus 40 rescue upon cell fusion.紫外线照射可诱导一种活性,该活性在细胞融合时刺激猿猴病毒40的拯救。
Mol Cell Biol. 1984 Jun;4(6):1159-62. doi: 10.1128/mcb.4.6.1159-1162.1984.
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Analysis of minimal functions of simian virus 40. II. Enhancement of oncogenic transformation in vitro by UV irradiation.猴病毒40的最小功能分析。II.紫外线照射对体外致癌转化的增强作用。
J Virol. 1973 Dec;12(6):1265-71. doi: 10.1128/JVI.12.6.1265-1271.1973.
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Isolation of defective lysogens from Simian virus 40-transformed mouse kidney cultures.从猿猴病毒40转化的小鼠肾培养物中分离缺陷性溶原菌。
J Virol. 1968 Nov;2(11):1272-82. doi: 10.1128/JVI.2.11.1272-1282.1968.
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Further evidence that ultraviolet radiation-enhanced reactivation of simian virus 40 in monkey kidney cells is not accompanied by mutagenesis.进一步的证据表明,紫外线辐射增强猴肾细胞中猿猴病毒40的复活并不伴随着诱变作用。
Mutat Res. 1982 Nov;105(5):291-8. doi: 10.1016/0165-7992(82)90095-1.
10
Effect of mitomycin C and 60Co gamma-irradiation on the replication of SV40 in cell lines of varying permissivity for SV40 replication.
J Gen Virol. 1979 Apr;43(1):235-9. doi: 10.1099/0022-1317-43-1-235.

引用本文的文献

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Replication of adeno-associated virus in cells irradiated with UV light at 254 nm.腺相关病毒在254纳米紫外线照射的细胞中的复制。
J Virol. 1989 Mar;63(3):1023-30. doi: 10.1128/JVI.63.3.1023-1030.1989.
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Inducible cellular responses to ultraviolet light irradiation and other mediators of DNA damage in mammalian cells.哺乳动物细胞对紫外线照射及其他DNA损伤介质的诱导性细胞反应。
Cell Biol Toxicol. 1990 Jan;6(1):105-26. doi: 10.1007/BF00135030.
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Origin of adeno-associated virus DNA replication is a target of carcinogen-inducible DNA amplification.
J Virol. 1991 Jun;65(6):3175-84. doi: 10.1128/JVI.65.6.3175-3184.1991.