Tol Menno B, Morales Angeles Danae, Scheffers Dirk-Jan
Department of Molecular Microbiology, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Groningen, The Netherlands.
Department of Molecular Microbiology, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Groningen, The Netherlands
Antimicrob Agents Chemother. 2015;59(6):3683-6. doi: 10.1128/AAC.04781-14. Epub 2015 Apr 13.
Nisin and related lantibiotics kill bacteria by pore formation or by sequestering lipid II. Some lantibiotics sequester lipid II into clusters, which were suggested to kill cells through delocalized peptidoglycan synthesis. Here, we show that cluster formation is always concomitant with (i) membrane pore formation and (ii) membrane depolarization. Nisin variants that cluster lipid II kill L-form bacteria with similar efficiency, suggesting that delocalization of peptidoglycan synthesis is not the primary killing mechanism of these lantibiotics.
乳链菌肽及相关羊毛硫抗生素通过形成孔道或螯合脂磷壁酸质Ⅱ来杀死细菌。一些羊毛硫抗生素将脂磷壁酸质Ⅱ螯合形成聚集体，有人认为这些聚集体通过使肽聚糖合成离位来杀死细胞。在此，我们表明聚集体的形成总是伴随着（i）膜孔道的形成和（ii）膜去极化。能使脂磷壁酸质Ⅱ形成聚集体的乳链菌肽变体以相似的效率杀死L型细菌，这表明肽聚糖合成的离位不是这些羊毛硫抗生素的主要杀菌机制。
