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T4噬菌体空壳感染细胞的代谢:噬菌体及空壳对大肠杆菌B中碳水化合物摄取的影响

Metabolism of T4 bacteriophage ghost-infected cells: effect of bacteriophage and ghosts on the uptake of carbohydrates in Escherichia coli B.

作者信息

Winkler H H, Duckworth D H

出版信息

J Bacteriol. 1971 Jul;107(1):259-67. doi: 10.1128/jb.107.1.259-267.1971.

DOI:10.1128/jb.107.1.259-267.1971
PMID:4935322
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC246913/
Abstract

Ghosts of T4 bacteriophage inhibit the uptake of thiomethyl-beta-galactoside (TMG), alpha-methylglucoside, glucose-6-phosphate, and glycerol in Escherichia coli B. The transport of orthonitrophenyl-beta-galactoside (ONPG) is also inhibited to a lesser degree and without alteration of the apparent K(m) of transport. These effects of ghosts parallel those of energy poisons on these systems. However, no one energy poison can produce such pronounced inhibitory effects in all these systems. The effect of the intact phage in these systems was either absent or very slight relative to the ghost. The effect of ghosts on the uptake of TMG was not immediate; at 10 C, no effect of the ghosts was apparent for at least 2 min. This suggests that a step, more temperature dependent than the attachment of the ghost, is necessary for the inhibitory action. The intracellular level of adenosine triphosphate (ATP) in the ghost-infected cells fell to less than 25% of the control value, and the ATP lost from the cell appeared in extracellular medium. Phage, on the other hand, caused no decrease in the intracellular ATP level. This loss of ATP from the cells after ghost infection suggests an alteration of the barrier properties of the membrane so that ATP can leave the cell; however, the accessibility of extracellular ONPG to intracellular beta-galactosidase does not increase. The dissimilarity of the actions of phage and ghosts on all properties examined does not support the model that the initial events in their infections are identical but that the intact phage, unlike the ghost, can provide information for the repair of its effects.

摘要

T4噬菌体的“幽灵”颗粒抑制大肠杆菌B中硫代甲基-β-半乳糖苷(TMG)、α-甲基葡萄糖苷、6-磷酸葡萄糖和甘油的摄取。对邻硝基苯基-β-半乳糖苷(ONPG)的转运也有较小程度的抑制,且不改变转运的表观米氏常数(K(m))。“幽灵”颗粒的这些作用与能量毒物对这些系统的作用相似。然而,没有一种能量毒物能在所有这些系统中产生如此显著的抑制作用。相对于“幽灵”颗粒,完整噬菌体在这些系统中的作用要么不存在,要么非常轻微。“幽灵”颗粒对TMG摄取的作用不是即时的;在10℃时,至少2分钟内“幽灵”颗粒没有明显作用。这表明,对于抑制作用来说,存在一个比“幽灵”颗粒附着更依赖温度的步骤。被“幽灵”颗粒感染的细胞中三磷酸腺苷(ATP)的细胞内水平降至对照值的25%以下,且从细胞中损失的ATP出现在细胞外培养基中。另一方面,噬菌体不会导致细胞内ATP水平下降。“幽灵”颗粒感染后细胞中ATP的这种损失表明细胞膜的屏障特性发生了改变,使得ATP能够离开细胞;然而,细胞外ONPG对细胞内β-半乳糖苷酶的可及性并未增加。噬菌体和“幽灵”颗粒在所有检测特性上作用的差异不支持这样一种模型,即它们感染的初始事件是相同的,但完整噬菌体与“幽灵”颗粒不同,能够提供修复其影响的信息。

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Assay for the Killing Properties of T2 Bacteriophage and Their "Ghosts".T2噬菌体及其“幽灵”的杀伤特性检测
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