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噬菌体SP82G对枯草芽孢杆菌细胞内脱氧核糖核酸失活过程的抑制作用。

Bacteriophage SP82G inhibition of an intracellular deoxyribonucleic acid inactivation process in Bacillus subtilis.

作者信息

McAllister W T, Green D M

出版信息

J Virol. 1972 Jul;10(1):51-9. doi: 10.1128/JVI.10.1.51-59.1972.

DOI:10.1128/JVI.10.1.51-59.1972
PMID:4625174
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC356424/
Abstract

The stability of SP82G bacteriophage deoxyribonucleic acid (DNA) after its uptake by competent Bacillus subtilis was examined by determining the ability of superinfecting phage particles to rescue genetic markers carried by the infective DNA. These experiments show that a DNA inactivation process within the cell is inhibited after infection of the cell by intact phage particles. The inhibition is maximally expressed 6 min after phage infection and is completely prevented by the addition of chloramphenicol at the time of infection. The protective effect of this function extends even to infective DNA which was present in the cell before the addition of intact phage. Continued protein synthesis does not appear to be a requirement for the maintenance of the inhibition. In an analogous situation, if infectious centers resulting from singly infecting phage particles are exposed to chloramphenicol shortly after the time of infection, an exponential decrease in the survival of infectious centers with time held in chloramphenicol is observed. If the addition of chloramphenicol is delayed until 6 min after infection, the infectious centers are resistant to chloramphenicol. The sensitivity of infectious centers treated with chloramphenicol at early times after infection is strongly dependent upon the multiplicity of infection and is consistent with a model of multiplicity reactivation. These results indicate that injected DNA is also susceptible to the intracellular inactivation process and suggest that the inhibition of this system is necessary for the successful establishment of an infectious center.

摘要

通过测定超感染噬菌体颗粒拯救感染性DNA携带的遗传标记的能力,研究了SP82G噬菌体脱氧核糖核酸(DNA)被感受态枯草芽孢杆菌摄取后的稳定性。这些实验表明,完整噬菌体颗粒感染细胞后,细胞内的DNA失活过程受到抑制。这种抑制在噬菌体感染后6分钟时最大程度地表现出来,并且在感染时添加氯霉素可完全阻止这种抑制。该功能的保护作用甚至扩展到添加完整噬菌体之前细胞中存在的感染性DNA。持续的蛋白质合成似乎不是维持这种抑制所必需的。在类似情况下,如果单感染噬菌体颗粒产生的感染中心在感染后不久暴露于氯霉素,则观察到感染中心的存活率随在氯霉素中保存的时间呈指数下降。如果氯霉素的添加延迟到感染后6分钟,则感染中心对氯霉素具有抗性。感染后早期用氯霉素处理的感染中心的敏感性强烈依赖于感染复数,并且与多重复活模型一致。这些结果表明,注入的DNA也易受细胞内失活过程影响,并表明抑制该系统对于成功建立感染中心是必要的。

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本文引用的文献

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