Kennell D
J Virol. 1970 Aug;6(2):208-17. doi: 10.1128/JVI.6.2.208-217.1970.
Two gene clusters on the Escherichia coli chromosome were induced at early times after T4 infection when >99% of the cells were infected: the lactose (lac) operon and prophage lambda. Their messenger ribonucleic acid (mRNA) was detected by hybridization to phi80 dlac deoxyribonucleic acid (DNA) and lambdaDNA, respectively. Synthesis of host mRNA could be initiated during the first few minutes after T4 infection, although no beta-galactosidase activity could be detected. Hybridization analyses of selected fractions from sucrose gradients revealed that most of this lac mRNA induced at very early times of T4 infection was not associated with ribosomes. In contrast, virtually all lac mRNA in uninfected bacteria was associated with polysomes. This exclusion affected all host mRNA; about 70% of E. coli(3)H-mRNA, labeled from 2 to 3 min after T4 infection, was excluded from polysomes. Infection even reduced the yield of beta-galactosidase from lac mRNA induced before infection. Gradients from rifampicin-inhibited cells showed the normal growth of lac mRNA polysomes; in contrast, T4 infection prevented growth of the preinduced lac polysomes. It is concluded that T4 infection interferes within seconds with the reassociation of ribosomes to host mRNA.
在T4感染后早期,当超过99%的细胞被感染时,大肠杆菌染色体上的两个基因簇被诱导表达:乳糖(lac)操纵子和原噬菌体λ。它们的信使核糖核酸(mRNA)分别通过与φ80 dlac脱氧核糖核酸(DNA)和λDNA杂交来检测。尽管在T4感染后的最初几分钟内检测不到β-半乳糖苷酶活性,但宿主mRNA的合成仍可启动。对蔗糖梯度中选定组分的杂交分析表明,在T4感染的极早期诱导产生的大部分lac mRNA不与核糖体结合。相比之下,未感染细菌中的几乎所有lac mRNA都与多核糖体结合。这种排斥作用影响了所有宿主mRNA;在T4感染后2至3分钟标记的约70%的大肠杆菌(3)H-mRNA被排除在多核糖体之外。感染甚至降低了感染前诱导产生的lac mRNA所产生的β-半乳糖苷酶的产量。来自利福平抑制细胞的梯度显示lac mRNA多核糖体正常生长;相反,T4感染阻止了预先诱导的lac多核糖体的生长。结论是,T4感染在几秒钟内就干扰了核糖体与宿主mRNA的重新结合。