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肺炎球菌中噬菌体诱导裂解的机制。

Mechanism of phage-induced lysis in pneumococci.

作者信息

Garcia P, Lopez R, Ronda C, Garcia E, Tomasz A

出版信息

J Gen Microbiol. 1983 Feb;129(2):479-87. doi: 10.1099/00221287-129-2-479.

Abstract

Earlier studies have suggested the possible role of host autolytic enzyme in the release of progeny phage from Dp-1 infected pneumococci. Several new experiments described here reinforce this notion. Specifically, the resistance of an autolysis-defective mutant to infection at low phage to cell ratios could be eliminated by prior 'coating' of the host bacteria with pneumococcal autolysin isolated from wild-type cells. Similar, productive infection was also possible by lowering the temperature of incubation to 30 degrees C, a condition that leads to a partial activation of the thermosensitive residual autolysin in the mutant cells. Other experiments, however, clearly indicate the role of the newly discovered phage-associated lysin (PAL), reported in the accompanying communication, in bacteriophage release and culture lysis; specifically, lysis was stimulated by reducing agents and inhibited by cardiolipin. It seems that both the host-related and the PAL activities are involved with Dp-1 induced lysis of pneumococci.

摘要

早期研究表明,宿主自溶酶在子代噬菌体从感染Dp-1的肺炎球菌中释放过程中可能发挥作用。本文所述的几个新实验强化了这一观点。具体而言,自溶缺陷型突变体在低噬菌体与细胞比例下对感染的抗性可通过先用从野生型细胞中分离出的肺炎球菌自溶素“包被”宿主细菌来消除。类似地,将孵育温度降至30摄氏度也可实现有效感染,此条件会导致突变体细胞中热敏性残余自溶素部分激活。然而,其他实验清楚地表明,随附通讯中报道的新发现的噬菌体相关溶素(PAL)在噬菌体释放和培养物裂解中发挥作用;具体而言,还原剂可刺激裂解,而心磷脂则抑制裂解。似乎宿主相关活性和PAL活性都与Dp-1诱导的肺炎球菌裂解有关。

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