Brey R N
J Bacteriol. 1982 Jan;149(1):306-15. doi: 10.1128/jb.149.1.306-315.1982.
Interaction of either colicin A or E1 with the surface of Escherichia coli cells resulted in extensive cleavage of the colicins into many peptide fragments in the molecular weight range of 10,000 to 30,000 released into the supernatants of colicin-cell mixtures. The protease inhibitor P-aminobenzamidine inhibited the cleavage of colicin A and enhanced colicin killing activity, suggesting that proteolysis is not required for the killing action of colicin. Fragments derived from the supernatants of the mixtures were inactive against sensitive cells. Proteolytic activity against both colicins was localized primarily in the outer membrane fraction of the cell envelope. At least two distinct protease activities appear to be present. Examination of the patterns of cleavage and inactivation of the colicins by a series of resistant mutants indicates that specific colicin receptors play no essential role in colicin proteolysis. In addition, evidence is presented that adsorption of colicin to specific receptors is a reversible process.
大肠菌素A或E1与大肠杆菌细胞表面相互作用,导致大肠菌素在分子质量范围为10,000至30,000的许多肽片段中被广泛裂解,这些片段释放到大肠菌素 - 细胞混合物的上清液中。蛋白酶抑制剂对氨基苯甲脒抑制大肠菌素A的裂解并增强大肠菌素的杀伤活性,这表明蛋白水解对于大肠菌素的杀伤作用不是必需的。混合物上清液中衍生的片段对敏感细胞无活性。针对两种大肠菌素的蛋白水解活性主要定位于细胞膜的外膜部分。似乎至少存在两种不同的蛋白酶活性。通过一系列抗性突变体对大肠菌素的裂解和失活模式进行检查表明,特定的大肠菌素受体在大肠菌素蛋白水解中不起重要作用。此外,有证据表明大肠菌素与特定受体的吸附是一个可逆过程。