Davies E A, Falahee M B, Adams M R
School of Biological Sciences, University of Surrey, Guildford, UK.
J Appl Bacteriol. 1996 Aug;81(2):139-46. doi: 10.1111/j.1365-2672.1996.tb04491.x.
The involvement of the cell wall in the acquisition of nisin resistance by Listeria monocytogenes F6861 and its nisin-resistant mutant was investigated. Results indicated that without a cell wall, the acquired nisin resistance of the mutant was lost. Cell surface hydrophobicity was shown to correlate with nisin sensitivity; the wild type strain being more hydrophobic than its mutant. The possible role of S-layer proteins in nisin resistance was investigated. Examination of strains by freeze-etching and atomic force microscopy did not demonstrate the presence of S-layers in either strain while SDS-PAGE following S-layer extraction procedures revealed no major protein bands. Chloramphenicol did not adversely affect the frequency of isolation of nisin-resistant mutants, indicating that de novo protein synthesis was not involved. The involvement of other cell surface components, teichoic and lipoteichoic acids, was also examined. In contrast with other reports, comparison of the total phospholipid content of the mutant with its parental strain showed no significant difference (P > 0.05).
研究了细胞壁在单核细胞增生李斯特菌F6861及其乳链菌肽抗性突变体获得乳链菌肽抗性中的作用。结果表明，没有细胞壁时，突变体获得的乳链菌肽抗性丧失。细胞表面疏水性与乳链菌肽敏感性相关；野生型菌株比其突变体更疏水。研究了S层蛋白在乳链菌肽抗性中的可能作用。通过冷冻蚀刻和原子力显微镜检查菌株，未在任何一种菌株中发现S层的存在，而采用S层提取程序后的SDS-PAGE未显示主要蛋白条带。氯霉素对乳链菌肽抗性突变体的分离频率没有不利影响，表明不涉及从头蛋白质合成。还检查了其他细胞表面成分，磷壁酸和脂磷壁酸的作用。与其他报道相反，突变体与其亲本菌株的总磷脂含量比较没有显著差异（P>0.05）。
