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噬菌体T1感染后信使核糖核酸的合成

Synthesis of messenger ribonucleic acid after bacteriophage T1 infection.

作者信息

Male C J, Christensen J R

出版信息

J Virol. 1970 Dec;6(6):727-37. doi: 10.1128/JVI.6.6.727-737.1970.

Abstract

Synthesis of host-specific and phage-specific messenger ribonucleic acid (mRNA) was studied in bacteria infected by unmodified (T1 . B) or modified [T1 . B(P1)] bacteriophage T1. In a "standard" infection of Escherichia coli B by T1 . B (no host-controlled modification involved), the rate and amount of T1 mRNA synthesis was intermediate between those values reported for infections by a virulent phage such as T4 or a temperate phage such as lambda. The initial rate of mRNA synthesis was slightly increased after T1 . B(P1) infection of E. coli B in comparison with T1 . B infection of the same host. Little or no phage mRNA synthesis could be detected in T1 . B infection of E. coli B(P1). Phage mRNA synthesis in T1 . B(P1)-infected E. coli B(P1) cells was approximately the same in amount as that seen in T1 . B(P1) infection of E. coli B. Synthesis of host-specific mRNA continued throughout the latent period in all infections studied. However, the enzyme beta-galactosidase could not be induced, except after T1 . B infection of E. coli B(P1). In an attempt to understand the apparent differences in mRNA synthesis after infection of E. coli B by phages T1 . B or T1 . B(P1), the effect of altered T1 deoxyribonucleic acid (DNA) methylation on mRNA synthesis was studied. Methyl-deficient T1 DNA, made in cells infected with ultraviolet-irradiated phage T3, inhibited (14)C-uridine incorporation more strongly than normal T1. One passage of methyl-deficient T1 through E. coli B restored uracil incorporation rates to those seen with ordinary T1. This suggests that methylation of T1 DNA can influence the rate of phage mRNA synthesis. However, attempts to relate the difference in mRNA synthesis seen between T1 . B and T1 . B(P1) in E. coli B to the activity of the P1 modification gene were not conclusive.

摘要

在被未修饰的(T1.B)或修饰的[T1.B(P1)]噬菌体T1感染的细菌中,研究了宿主特异性和噬菌体特异性信使核糖核酸(mRNA)的合成。在T1.B对大肠杆菌B进行的“标准”感染(不涉及宿主控制的修饰)中,T1 mRNA合成的速率和量介于烈性噬菌体(如T4)或温和噬菌体(如λ)感染所报道的值之间。与T1.B感染同一宿主相比,T1.B(P1)感染大肠杆菌B后,mRNA合成的初始速率略有增加。在T1.B感染大肠杆菌B(P1)时,几乎检测不到或检测不到噬菌体mRNA的合成。在T1.B(P1)感染的大肠杆菌B(P1)细胞中,噬菌体mRNA的合成量与T1.B(P1)感染大肠杆菌B时的合成量大致相同。在所有研究的感染中,宿主特异性mRNA的合成在整个潜伏期持续进行。然而,除了T1.B感染大肠杆菌B(P1)后,β-半乳糖苷酶无法被诱导。为了理解噬菌体T1.B或T1.B(P1)感染大肠杆菌B后mRNA合成的明显差异,研究了T1脱氧核糖核酸(DNA)甲基化改变对mRNA合成的影响。在感染紫外线照射的噬菌体T3的细胞中产生的甲基缺陷型T1 DNA比正常T1更强烈地抑制(14)C-尿苷掺入。甲基缺陷型T1在大肠杆菌B中传代一次后,尿嘧啶掺入率恢复到普通T1的水平。这表明T1 DNA的甲基化可以影响噬菌体mRNA的合成速率。然而,试图将大肠杆菌B中T1.B和T1.B(P1)之间mRNA合成的差异与P1修饰基因的活性联系起来的尝试并不具有决定性。

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