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1
Synthesis of an S-adenosylmethionine-cleaving enzyme in T3-infected Escherichia coli and its disturbance by co-infection with enzymatically incompetent bacteriophage.在T3感染的大肠杆菌中S-腺苷甲硫氨酸裂解酶的合成及其与无酶活性噬菌体共感染对其的干扰。
J Virol. 1967 Feb;1(1):57-63. doi: 10.1128/jvi.1.1.57-63.1967.
2
Synthesis of bacteriophage-coded gene products during infection of Escherichia coli with amber mutants of T3 and T7 defective in gene 1.用T3和T7基因1有缺陷的琥珀突变体感染大肠杆菌期间噬菌体编码基因产物的合成。
J Virol. 1973 Apr;11(4):465-72. doi: 10.1128/JVI.11.4.465-472.1973.
3
Control of gene function in bacteriophage Tr. 3. Preventing the shutoff of early enzyme synthesis.噬菌体Tr中基因功能的控制。3. 防止早期酶合成的关闭。
J Virol. 1971 Nov;8(5):613-8. doi: 10.1128/JVI.8.5.613-618.1971.
4
Effect of infection with T-even phage on the inducible synthesis of beta-glactosidase in Escherichia coli.T-偶数噬菌体感染对大肠杆菌中β-半乳糖苷酶诱导合成的影响。
J Mol Biol. 1967 Aug 14;27(3):453-68. doi: 10.1016/0022-2836(67)90051-4.
5
[Synthesis of phage coded products during infection of E. coli in gene-1-mutants of phages T3 and T7].[噬菌体T3和T7基因1突变体感染大肠杆菌期间噬菌体编码产物的合成]
Hoppe Seylers Z Physiol Chem. 1972 Oct;353(10):1530.
6
T3 and T7 bacteriophage deoxyribonucleic acid-directed enzyme synthesis in vitro.T3和T7噬菌体脱氧核糖核酸体外指导的酶合成
J Virol. 1970 Dec;6(6):750-3. doi: 10.1128/JVI.6.6.750-753.1970.
7
SAMase gene of bacteriophage T3 is responsible for overcoming host restriction.噬菌体T3的SAMase基因负责克服宿主限制。
J Virol. 1976 Jul;19(1):136-45. doi: 10.1128/JVI.19.1.136-145.1976.
8
Bacteriophage T3 and T7 early RNAs are translated by eukaryotic 80S ribosomes: active phage T3 coded S-adenosylmethionine cleaving enzyme is synthesized.噬菌体T3和T7早期RNA由真核80S核糖体翻译：合成了有活性的噬菌体T3编码的S-腺苷甲硫氨酸裂解酶。
Proc Natl Acad Sci U S A. 1976 Aug;73(8):2752-6. doi: 10.1073/pnas.73.8.2752.
9
Negative control of protein synthesis after infection with bacteriophage T7.噬菌体T7感染后蛋白质合成的负调控
Proc Natl Acad Sci U S A. 1972 Aug;69(8):2203-7. doi: 10.1073/pnas.69.8.2203.
10
In vivo suppression of coding associated with bacteriophage-induced S-adenosylmethionine hydrolase.体内对与噬菌体诱导的S-腺苷甲硫氨酸水解酶相关编码的抑制作用。
J Bacteriol. 1970 Feb;101(2):398-407. doi: 10.1128/jb.101.2.398-407.1970.

引用本文的文献

1
Structure and mechanism of a phage-encoded SAM lyase revises catalytic function of enzyme family.噬菌体编码的 SAM 裂解酶的结构与机制修正了酶家族的催化功能。
Elife. 2021 Feb 10;10:e61818. doi: 10.7554/eLife.61818.
2
Pre-early functions of bacteriophage T5 and its relatives.噬菌体T5及其相关噬菌体的早期前期功能。
Bacteriophage. 2015 Aug 25;5(4):e1086500. doi: 10.1080/21597081.2015.1086500. eCollection 2015 Oct-Dec.
3
Type I restriction enzymes and their relatives.I 型限制酶及其相关酶。
Nucleic Acids Res. 2014 Jan;42(1):20-44. doi: 10.1093/nar/gkt847. Epub 2013 Sep 24.
4
Abortive infection of F-plasmid-containing Escherichia coli cells by bacterial virus T7 is determined by the right end of T7 gene 1.含F质粒的大肠杆菌细胞被细菌病毒T7的流产感染由T7基因1的右端决定。
J Virol. 1983 Apr;46(1):293-6. doi: 10.1128/JVI.46.1.293-296.1983.
5
Bacteriophage survival: multiple mechanisms for avoiding the deoxyribonucleic acid restriction systems of their hosts.噬菌体的存活：避免宿主脱氧核糖核酸限制系统的多种机制。
Microbiol Rev. 1983 Sep;47(3):345-60. doi: 10.1128/mr.47.3.345-360.1983.
6
Influence of phage T3 and T7 gene functions on a type III(EcoP1) DNA restriction-modification system in vivo.噬菌体T3和T7基因功能对III型（EcoP1）DNA限制修饰系统的体内影响。
Mol Gen Genet. 1982;185(3):457-61. doi: 10.1007/BF00334140.
7
Bacteriophage T3 and bacteriophage T7 virus-host cell interactions.噬菌体T3与噬菌体T7的病毒-宿主细胞相互作用。
Microbiol Rev. 1981 Mar;45(1):9-51. doi: 10.1128/mr.45.1.9-51.1981.
8
Control of gene function in bacteriophage Tr. 3. Preventing the shutoff of early enzyme synthesis.噬菌体Tr中基因功能的控制。3. 防止早期酶合成的关闭。
J Virol. 1971 Nov;8(5):613-8. doi: 10.1128/JVI.8.5.613-618.1971.
9
Amber mutants of bacteriophages T3 and T7 defective in phage-directed deoxyribonucleic acid synthesis.噬菌体T3和T7的琥珀突变体在噬菌体指导的脱氧核糖核酸合成方面存在缺陷。
J Virol. 1967 Aug;1(4):779-92. doi: 10.1128/JVI.1.4.779-792.1967.
10
Physiological and genetic aspects of abortive infection of a Shigella sonnei strain by coliphage T7.大肠杆菌噬菌体T7对宋内志贺氏菌菌株流产感染的生理学和遗传学方面
J Virol. 1968 Apr;2(4):335-45. doi: 10.1128/JVI.2.4.335-345.1968.

本文引用的文献

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INHIBITION OF THYMIDINE KINASE FORMATION IN LM (TK-) CELLS SIMULTANEOUSLY INFECTED WITH VACCINIA AND A THYMIDINE KINASELESS VACCINIA MUTANT.在同时感染痘苗病毒和胸苷激酶缺陷型痘苗病毒突变体的LM（TK-）细胞中胸苷激酶形成的抑制作用
Virology. 1965 Jun;26:374-7. doi: 10.1016/0042-6822(65)90287-4.
2
THE ENZYMATIC METHYLATION OF RNA AND DNA. 8. EFFECTS OF BACTERIOPHAGE INFECTION ON THE ACTIVITY OF THE METHYLATING ENZYMES.RNA和DNA的酶促甲基化。8. 噬菌体感染对甲基化酶活性的影响。
Proc Natl Acad Sci U S A. 1964 Aug;52(2):292-7. doi: 10.1073/pnas.52.2.292.
3
MUTANT STRAINS OF HERPES SIMPLEX DEFICIENT IN THYMIDINE KINASE-INDUCING ACTIVITY.胸苷激酶诱导活性缺陷的单纯疱疹突变株。
Virology. 1964 Apr;22:493-502. doi: 10.1016/0042-6822(64)90070-4.
4
ISOLATION AND PROPERTIES OF VACCINIA MUTANTS DEFICIENT IN THYMIDINE KINASE-INDUCING ACTIVITY.胸苷激酶诱导活性缺陷的痘苗突变体的分离与特性
Virology. 1964 Feb;22:214-25. doi: 10.1016/0042-6822(64)90006-6.
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BACTERIOPHAGE REPRODUCTION.噬菌体繁殖
Annu Rev Microbiol. 1963;17:87-114. doi: 10.1146/annurev.mi.17.100163.000511.
6
THYMIDINE-REQUIRING MUTANTS OF PHAGE T4.噬菌体T4的胸腺嘧啶核苷需求型突变体
Proc Natl Acad Sci U S A. 1963 Sep;50(3):526-32. doi: 10.1073/pnas.50.3.526.
7
The formation of galactokinase in cells of Escherichia coli after infection with the transducing lambda bacteriophage.用转导性λ噬菌体感染大肠杆菌细胞后半乳糖激酶的形成。
J Mol Biol. 1963 Feb;6:128-36. doi: 10.1016/s0022-2836(63)80128-x.
8
The ability of irradiated bacteriophage T2 to initiate the synthesis of deoxycytidylate hydroxymethylase in Escherichia coli.经辐射的噬菌体T2在大肠杆菌中启动脱氧胞苷酸羟甲基化酶合成的能力。
Virology. 1961 Feb;13:242-8. doi: 10.1016/0042-6822(61)90058-7.
9
Genetic recombination and replication in bacteriophage.噬菌体中的基因重组与复制
J Cell Physiol Suppl. 1955 May;45(Suppl. 2):51-74. doi: 10.1002/jcp.1030450505.
10
The enzymatic methylation of ribonucleic acid and deoxyribonucleic acid. X. Bacteriophage T3-induced S-adenosylmethionine cleavage.核糖核酸和脱氧核糖核酸的酶促甲基化作用。X. 噬菌体T3诱导的S-腺苷甲硫氨酸裂解
J Biol Chem. 1966 May 10;241(9):1995-2006.

在T3感染的大肠杆菌中S-腺苷甲硫氨酸裂解酶的合成及其与无酶活性噬菌体共感染对其的干扰。

Synthesis of an S-adenosylmethionine-cleaving enzyme in T3-infected Escherichia coli and its disturbance by co-infection with enzymatically incompetent bacteriophage.

作者信息

Hausmann R

出版信息

J Virol. 1967 Feb;1(1):57-63. doi: 10.1128/jvi.1.1.57-63.1967.

DOI:10.1128/jvi.1.1.57-63.1967
PMID:4918233
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC375505/
Abstract

Synthesis of an S-adenosylmethionine-cleaving enzyme evoked by infection of Escherichia coli with phage T3 was independent of the multiplicity of infection with the wild type, T3 sam(+). It was depressed, however, by mixed infection with related phages genetically incapable of directing enzyme production, such as T3 sam(-), or phage T7. The depressor effect of enzymatically incompetent genomes depended on their proportion among the input phage and not on their absolute multiplicity. The effect was more pronounced with homologous, enzymatically incompetent phage (T3 sam(-)) than with heterologous phage (T7). After ultraviolet irradiation, enzymatically incompetent genomes lost their depressing power; at a survival level of 10(-7), no depression by either homologous or heterologous phage upon T3 sam(+)-directed enzyme synthesis was detected.

摘要

噬菌体T3感染大肠杆菌所诱发的S-腺苷甲硫氨酸裂解酶的合成，与野生型T3 sam(+)的感染复数无关。然而，与在遗传上不能指导酶产生的相关噬菌体，如T3 sam(-)或噬菌体T7混合感染时，该酶的合成受到抑制。无酶活性基因组的抑制作用取决于它们在输入噬菌体中的比例，而不取决于它们的绝对感染复数。同源的无酶活性噬菌体（T3 sam(-)）比异源噬菌体（T7）的这种抑制作用更明显。紫外线照射后，无酶活性基因组失去其抑制能力；在存活率为10^(-7)时，未检测到同源或异源噬菌体对T3 sam(+)指导的酶合成有抑制作用。