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Host transcription in bacteriophage P22-infected Salmonella typhimurium.

机译:在噬菌体P22感染沙门氏菌中的宿主转录。

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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.
机译:通过脉冲标记动力学和RNA-DNA杂交测量的宿主RNA合成的动力学在感染后不久被抑制了10倍,抑制了噬菌体P22。这种早期抑制持续到前6分钟的感染,不仅影响RNA合成,而且影响其他几种需要蜂窝功能。在溶血性感染中,细菌转录速率迅速恢复到未感染的对照的价值。在裂解感染中,宿主转录的速率仅增加到原始水平的约20%至25%,表明抑制裂解反应中RNA合成的第二种机制。早期抑制是多样性依赖性,植物蛋白酰基因不敏感,且含有噬菌体基因24的依赖性。裂解抑制取决于基因24的表达但与基因23无关。

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