乳酸链球菌素
乳酸乳球菌
脂磷壁酸
脂质Ⅱ
细胞壁
化学
生物化学
拉伤
细菌
肽聚糖
生物
微生物学
乳酸
抗菌剂
金黄色葡萄球菌
解剖
遗传学
作者
Naomi E. Kramer,Hester E. Hasper,Patrick T. C. van den Bogaard,Siegfried Morath,Ben de Kruijff,Thomas Härtung,Eddy J. Smid,Eefjan Breukink,Jan Kok,Oscar P. Kuipers
出处
期刊:Microbiology
[Microbiology Society]
日期:2008-06-01
卷期号:154 (6): 1755-1762
被引量:53
标识
DOI:10.1099/mic.0.2007/015412-0
摘要
Nisin is a post-translationally modified antimicrobial peptide produced by Lactococcus lactis which binds to lipid II in the membrane to form pores and inhibit cell-wall synthesis. A nisin-resistant (NisR) strain of L. lactis, which is able to grow at a 75-fold higher nisin concentration than its parent strain, was investigated with respect to changes in the cell wall. Direct binding studies demonstrated that less nisin was able to bind to lipid II in the membranes of L. lactis NisR than in the parent strain. In contrast to vancomycin binding, which showed ring-like binding, nisin was observed to bind in patches close to cell-division sites in both the wild-type and the NisR strains. Comparison of modifications in lipoteichoic acid of the L. lactis strains revealed an increase in d-alanyl esters and galactose as substituents in L. lactis NisR, resulting in a less negatively charged cell wall. Moreover, the cell wall displays significantly increased thickness at the septum. These results indicate that shielding the membrane and thus the lipid II molecule, thereby decreasing abduction of lipid II and subsequent pore-formation, is a major defence mechanism of L. lactis against nisin.
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