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质粒控制的噬菌体λ脱氧核糖核酸中甲基化碱基含量的变异

Plasmid-controlled variation in the content of methylated bases in bacteriophage lambda deoxyribonucleic acid.

作者信息

Hattman S

出版信息

J Virol. 1972 Sep;10(3):356-61. doi: 10.1128/JVI.10.3.356-361.1972.

Abstract

The N(6)-methyladenine (MeAde) and 5-methylcytosine (MeC) contents in deoxyribonucleic acid (DNA) of bacteriophage lambda has been analyzed as a function of host specificity. The following facts have emerged: (i) lambda grown on strains harboring the P1 prophage contain ca. 70 more MeAde residues/DNA molecule than lambda grown either in the P1-sensitive parent, or in a P1 immune-defective lysogen which does not confer P1 modification; (ii) lambda grown on strains harboring the N-3 drug-resistance factor contain ca. 60 more MeC residues/DNA molecule than lambda grown on the parental strain lacking the factor; (iii) lambda grown in Escherichia coli B strains is devoid of MeC, whereas lambda grown in a B (N-3) host contains a high level of MeC; (iv) the MeAde content in lambda DNA is not affected by the N-3 factor. These results suggest that P1 controls an adenine-specific DNA methylase, and that the N-3 plasmid controls a cytosine-specific DNA methylase. The N-3 factor has been observed previously to direct cytosine-specific methylation of phage P22 DNA and E. coli B DNA in vivo; in vitro studies presented here demonstrate this activity.

摘要

已对噬菌体λ脱氧核糖核酸(DNA)中的N⁶-甲基腺嘌呤(MeAde)和5-甲基胞嘧啶(MeC)含量作为宿主特异性的函数进行了分析。出现了以下事实:(i)在携带P1原噬菌体的菌株上生长的λ,每个DNA分子含有的MeAde残基比在P1敏感亲本或不赋予P1修饰的P1免疫缺陷溶原菌中生长的λ多约70个;(ii)在携带N-3耐药因子的菌株上生长的λ,每个DNA分子含有的MeC残基比在缺乏该因子的亲本菌株上生长的λ多约60个;(iii)在大肠杆菌B菌株中生长的λ不含MeC,而在B(N-3)宿主中生长的λ含有高水平的MeC;(iv)λ DNA中的MeAde含量不受N-3因子的影响。这些结果表明,P1控制一种腺嘌呤特异性DNA甲基化酶,并且N-3质粒控制一种胞嘧啶特异性DNA甲基化酶。先前已观察到N-3因子在体内指导噬菌体P22 DNA和大肠杆菌B DNA的胞嘧啶特异性甲基化;此处给出的体外研究证明了这种活性。

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Methylation pattern of lambda deoxyribonucleic acid.λ 脱氧核糖核酸的甲基化模式
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The host specificity system in Escherichia coli SK.
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本文引用的文献

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THE CONTROL OF HOST-INDUCED MODIFICATION BY PHAGE P1.
Virology. 1964 Jun;23:270-1. doi: 10.1016/0042-6822(64)90291-0.

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