Suppr超能文献

呈扇形射出的规则排列的壁膜粒参与青霉素诱导的葡萄球菌死亡过程。

Fan-shaped ejections of regularly arranged murosomes involved in penicillin-induced death of staphylococci.

作者信息

Giesbrecht P, Kersten T, Wecke J

机构信息

Robert Koch-Institute of the Federal Health Office, Berlin, Germany.

出版信息

J Bacteriol. 1992 Apr;174(7):2241-52. doi: 10.1128/jb.174.7.2241-2252.1992.

Abstract

Electron microscopic research into the murosomes of staphylococci has shown that the number of murosomes involved in penicillin-induced death varies depending on the experimental conditions employed. With 0.1 micrograms of penicillin G per ml, only 1 of a total of about 20 murosomes, the "killing murosome," completely perforated the pressure-stabilized peripheral cell wall during a three-step process. This strictly localized event was mainly attributed to a mechanical effect being comparable to the process of aneurysm formation. Wall perforation was also considered to mark the very moment of penicillin-induced death ("nonlytic killing event"), while bacteriolysis started only postmortem. By varying the osmolarity of the growth medium, the number of murosomes involved in penicillin-induced killing increased considerably, which resulted in the ejection of a fan-shaped row of murosomes at the second division plane. These data are compatible with the finding that, in untreated or chloramphenicol-treated staphylococci, the activation of the murosomes resulted in (i) the formation of regularly arranged "blebs" on the cell surface, containing traces of disintegrated wall material, and (ii) the subsequent liberation of the murosomes lying underneath, leaving behind their former sites in the peripheral wall as a row of regularly arranged "pores" in every division plane. The number, distribution, and positioning of these blebs corresponded with those of the pores and the original murosomes. The significance of wall autolysins liberated from the first division plane for penicillin-induced wall perforation at the second division plane is discussed.

摘要

对葡萄球菌的胞壁质体进行的电子显微镜研究表明,参与青霉素诱导死亡的胞壁质体数量因所采用的实验条件而异。每毫升含有0.1微克青霉素G时,在总共约20个胞壁质体中,只有1个“致死胞壁质体”在一个三步过程中完全穿透了压力稳定的外周细胞壁。这一严格局限的事件主要归因于一种类似于动脉瘤形成过程的机械效应。壁穿孔也被认为标志着青霉素诱导死亡的那一刻(“非溶菌性杀伤事件”),而细菌溶解仅在死后开始。通过改变生长培养基的渗透压,参与青霉素诱导杀伤的胞壁质体数量大幅增加,这导致在第二个分裂平面上呈扇形排出一排胞壁质体。这些数据与以下发现相符:在未处理或氯霉素处理的葡萄球菌中,胞壁质体的激活导致(i)在细胞表面形成规则排列的“泡”,其中含有分解的壁物质痕迹,以及(ii)随后位于下方的胞壁质体释放,在外周壁的原位置留下一排规则排列的“孔”,位于每个分裂平面上。这些泡的数量、分布和定位与孔和原始胞壁质体的数量、分布和定位相对应。文中讨论了从第一个分裂平面释放的壁自溶素对第二个分裂平面上青霉素诱导的壁穿孔的意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82e5/205845/e49d8795852d/jbacter00073-0200-a.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验