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1
Evidence against phenotypic mixing between bacteriophage T4 wild type and T4v minus.反对噬菌体T4野生型和T4v减型之间表型混合的证据。
J Virol. 1974 Sep;14(3):592-7. doi: 10.1128/JVI.14.3.592-597.1974.
2
Nonreplicated DNA and DNA fragments in T4 r- bacteriophage particles: phenotypic mixing of a phage protein.T4 r-噬菌体颗粒中的非复制性DNA和DNA片段:一种噬菌体蛋白的表型混合
J Virol. 1974 Jun;13(6):1274-90. doi: 10.1128/JVI.13.6.1274-1290.1974.
3
Injection of ultraviolet-damage-specific enzyme by T4 bacteriophage.T4噬菌体注射紫外线损伤特异性酶。
J Virol. 1973 Jul;12(1):1-8. doi: 10.1128/JVI.12.1.1-8.1973.
4
Host- and phage-mediated repair of radiation damage in bacteriophage T4.宿主和噬菌体介导的噬菌体T4辐射损伤修复
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5
Deoxyribonucleic acid repair in bacteriophage T4: observations on the roles of the x and v genes and of host factors.噬菌体T4中的脱氧核糖核酸修复:关于x和v基因以及宿主因子作用的观察
J Virol. 1972 Oct;10(4):730-6. doi: 10.1128/JVI.10.4.730-736.1972.
6
Biochemical studies on radiation-sensitive mutations in bacteriophage T4-1.噬菌体T4-1辐射敏感突变的生化研究。
J Biochem. 1975 Feb;77(2):303-11. doi: 10.1093/oxfordjournals.jbchem.a130727.
7
The repair of ultraviolet damage by phage T4: the role of the early phage genes.噬菌体T4对紫外线损伤的修复:早期噬菌体基因的作用
Basic Life Sci. 1975;5A:143-7. doi: 10.1007/978-1-4684-2895-7_18.
8
Enzymic mechanism of excision-repair in T4-infected cells.T4 感染细胞中切除修复的酶促机制。
Basic Life Sci. 1975;5A:135-42. doi: 10.1007/978-1-4684-2895-7_17.
9
Ultraviolet reactivation and ultraviolet mutagenesis of infectious lambda DNA: strong inhibition by treatment of DNA in vitro with UV-endonuclease from Micrococcus luteus.感染性λ噬菌体DNA的紫外线复活与紫外线诱变:用藤黄微球菌的紫外线内切酶在体外处理DNA可产生强烈抑制作用。
Mutat Res. 1975 Feb;27(2):147-56. doi: 10.1016/0027-5107(75)90074-3.
10
Physical association of pyrimidine dimer DNA glycosylase and apurinic/apyrimidinic DNA endonuclease essential for repair of ultraviolet-damaged DNA.嘧啶二聚体DNA糖基化酶与脱嘌呤/脱嘧啶DNA内切核酸酶的物理关联对紫外线损伤DNA的修复至关重要。
Proc Natl Acad Sci U S A. 1981 May;78(5):2742-6. doi: 10.1073/pnas.78.5.2742.

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THE ROLE OF THYMINE DIMER IN THE PHOTO-INACTIVATION OF THE BACTERIOPHAGE T4V1.胸腺嘧啶二聚体在噬菌体T4V1光灭活中的作用。
J Mol Biol. 1963 Oct;7:431-41. doi: 10.1016/s0022-2836(63)80035-2.
2
Mutants of phage T4 with increased sensitivity to ultraviolet.对紫外线敏感性增强的噬菌体T4突变体。
Virology. 1963 Jan;19:66-71. doi: 10.1016/0042-6822(63)90025-4.
3
Incorporation of [14C]glycine into Micrococcus lysodeikticus membrane protein and effects of protein synthesis inhibitors.[14C]甘氨酸掺入溶壁微球菌膜蛋白及蛋白质合成抑制剂的作用
Biochim Biophys Acta. 1970 Mar 17;203(1):83-93. doi: 10.1016/0005-2736(70)90038-6.
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T4 endonuclease involved in repair of DNA.参与DNA修复的T4核酸内切酶。
Proc Natl Acad Sci U S A. 1970 Dec;67(4):1839-45. doi: 10.1073/pnas.67.4.1839.
5
Mechanism of repair of DNA in bacteriophage. II. Inability of ultraviolet-sensitive strains of bacteriophage in inducing an enzyme activity to excise pyrimidine dimers.噬菌体中DNA的修复机制。II. 紫外线敏感型噬菌体菌株诱导切除嘧啶二聚体的酶活性的无能。
J Mol Biol. 1970 Jan 28;47(2):243-55. doi: 10.1016/0022-2836(70)90343-8.
6
Mechanism of repair of DNA in bacteriophage. I. Excision of pyrimidine dimers from ultraviolet-irradiated DNA by an extract of T4-infected cells.噬菌体中DNA的修复机制。I. 用T4感染细胞的提取物从紫外线照射的DNA中切除嘧啶二聚体。
J Mol Biol. 1970 Jan 28;47(2):231-42. doi: 10.1016/0022-2836(70)90342-6.
7
Endonucleolytic cleavage of UV-irradiated DNA controlled by the V+ gene in phage T4.噬菌体T4中由V +基因控制的紫外线照射DNA的内切核酸酶切割。
Biochem Biophys Res Commun. 1969 Nov 6;37(4):646-51. doi: 10.1016/0006-291x(69)90859-6.
8
Analysis of photoenzymatic repair of UV lesions in DNA by single light flashes. II. In vivo studies with Escherichia coli cells and bacteriophage.通过单次闪光对DNA中紫外线损伤进行光酶修复的分析。II. 大肠杆菌细胞和噬菌体的体内研究
Mutat Res. 1968 Nov-Dec;6(3):371-85. doi: 10.1016/0027-5107(68)90054-7.
9
Recovery of UV-inactivated E. coli cells by the v-gene action of phage T4.
Mutat Res. 1968 Jul-Aug;6(1):175-9. doi: 10.1016/0027-5107(68)90115-2.
10
The process of infection with bacteriophage phi-X174. XIX. Isolation and characterization of a chloramphenicol-resistant protein from phi-X-infected cells.
J Mol Biol. 1968 Mar 28;32(3):567-78. doi: 10.1016/0022-2836(68)90343-4.

反对噬菌体T4野生型和T4v减型之间表型混合的证据。

Evidence against phenotypic mixing between bacteriophage T4 wild type and T4v minus.

作者信息

Chiang T, Harm W

出版信息

J Virol. 1974 Sep;14(3):592-7. doi: 10.1128/JVI.14.3.592-597.1974.

DOI:10.1128/JVI.14.3.592-597.1974
PMID:4604454
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC355554/
Abstract

In a recent publication Shames et al. (1973) concluded that the UV-specific T4 endonuclease (a repair enzyme coded for by the gene v of wild-type T4) is a component of extracellular phage, which is injected into the host cell and can perform an early repair step without requiring gene expression. This notion is, however, not supported by results presented in this paper. Lysates obtained from mixed multiple infection of Escherichia coli cells with T4v(1) (-) and T4v(+) (or T4v(2) (-) and T4v(+)) failed to show the expected phenotypic mixing, i.e., incorporation of UV endonuclease into capsids of v(-) phages resulting in recognizable repair. The fraction of v(+) and v(-) particles in such lysates was determined by single-plaque analysis before and after irradiation with a UV dose at which virtually all survivors are particles having undergone repair. Even though our mixed infection conditions were most favorable for the possible occurrence of phenotypic mixing, none out of several hundred individual plaques from survivors were found to be genotypically v(-), whereas 30 were expected in the case that phenotypically mixed v(-) particles were repaired like T4v(+). Our failure to observe phenotypic mixing suggests that the data by Shames et al. reflect intracellular synthesis of endonuclease after phage infection.

摘要

在最近的一篇论文中,沙姆斯等人(1973年)得出结论,紫外线特异性T4核酸内切酶(一种由野生型T4的基因v编码的修复酶)是细胞外噬菌体的一个组成部分,它被注入宿主细胞,并且无需基因表达就能执行早期修复步骤。然而,本文所呈现的结果并不支持这一观点。用T4v(1) (-) 和T4v(+)(或T4v(2) (-) 和T4v(+))对大肠杆菌细胞进行混合多重感染所获得的裂解物未能显示出预期的表型混合,即紫外线核酸内切酶掺入v(-)噬菌体的衣壳中从而导致可识别的修复。在以紫外线剂量照射前后,通过单斑分析来确定此类裂解物中v(+)和v(-)颗粒的比例,在该紫外线剂量下,几乎所有存活者都是经过修复的颗粒。尽管我们的混合感染条件最有利于可能发生的表型混合,但在数百个来自存活者的单个噬菌斑中,没有一个被发现基因型为v(-),而如果表型混合的v(-)颗粒像T4v(+)那样被修复,预计会有30个。我们未能观察到表型混合,这表明沙姆斯等人的数据反映了噬菌体感染后核酸内切酶的细胞内合成。