Pipas J M, Reeves R H
J Virol. 1979 Dec;32(3):822-31. doi: 10.1128/JVI.32.3.822-831.1979.
The kinetics of host RNA synthesis, as measured by pulse-label kinetics and RNA-DNA hybridization, is inhibited 10-fold shortly after infection with bacteriophage P22. This early inhibition lasts through the first 6 min of infection and affects not only RNA synthesis but several other energy-requiring cellular functions. In lysogenic infections, the rate of bacterial transcription rapidly recovers to the value of uninfected controls. In lytic infections, the rate of host transcription increases only to about 20 to 25% of the original level, indicating a second mechanism for the inhibition of RNA synthesis in the lytic response. The early inhibition is multiplicity dependent, bhloramphenicol insensitive, and independent of phage gene 24. The lytic inhibition is dependent upon the expression of gene 24 but independent of gene 23.
通过脉冲标记动力学和RNA-DNA杂交测定的宿主RNA合成动力学,在感染噬菌体P22后不久被抑制了10倍。这种早期抑制持续到感染后的前6分钟,不仅影响RNA合成,还影响其他几种需要能量的细胞功能。在溶原性感染中,细菌转录速率迅速恢复到未感染对照的值。在裂解性感染中,宿主转录速率仅增加到原始水平的约20%至25%,这表明在裂解反应中存在抑制RNA合成的第二种机制。早期抑制是多重复依赖性的,对氯霉素不敏感,并且与噬菌体基因24无关。裂解抑制依赖于基因24的表达,但与基因23无关。