Mechanism of lantibiotic-induced pore-formation
Mechanism of lantibiotic-induced pore-formation
复制标题
羊毛硫抗生素诱导的孔隙形成机制
DOI：
10.1007/bf00399423
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
A. Driessen
中科院分区：
文献类型：
--
作者：
G. Moll;G. Roberts;W. N. Konings;A. Driessen
乳链菌肽和其他羊毛硫抗生素对革兰氏阳性菌具有杀菌作用，并能抑制细菌芽孢的生长。杀菌作用似乎是由于细菌膜上孔的形成。在不存在阴离子膜磷脂的情况下，羊毛硫抗生素乳链菌肽充当阴离子选择性载体。在阴离子磷脂存在的情况下，乳链菌肽在细胞、蛋白脂质体、脂质体和黑色脂质膜中形成非选择性、瞬时的、多状态的孔。孔的形成涉及不同的步骤。首先，乳链菌肽与阴离子膜表面紧密结合，导致局部浓度较高。这导致磷脂极性头基-水界面附近的脂质动力学受到干扰，并且脂质被固定。在跨膜电位高于阈值水平的情况下，分子可能作为聚集体重新定向，从表面结合结构转变为膜插入结构。结合的阴离子磷脂的共同插入导致脂质表面弯曲，从而产生楔状、非特异性、充满水的孔。
Nisin and other lantibiotics have a bacteriocidal effect against Gram-positive bacteria, and also inhibit the outgrowth of bacterial spores. The bacteriocidal effect appears to be due to the formation of pores in the bacterial membrane. In the absence of anionic membrane phospholipids, the lantibiotic nisin acts as an anion selective carrier. In the presence of anionic phospholipids, nisin forms nonselective, transient, multi-state pores in cells, proteoliposomes, liposomes and black lipid membranes. Pore formation involves distinct steps. First, nisin associates tightly with the anionic membrane surface leading to a high local concentration. This results in a disturbance of the lipid dynamics near the phospholipid polar head group-water interface, and an immobilization of lipids. In the presence of a transmembrane electrical potential above the threshold level, the molecules reorient, presumably as an aggregate, from a surface-bound into a membrane-inserted configuration. Co-insertion of bound, anionic phospholipids results in bending of the lipid surface giving rise to a wedge-like, nonspecific, water-filled pore.