Center for Bacterial Cell Biology, Institute for Cell and Molecular Biosciences, Newcastle University, United Kingdom.
Annu Rev Microbiol. 2012;66:103-23. doi: 10.1146/annurev-micro-092611-150159.
Bacterial persistence is caused by the presence of rare, slowly growing bacteria among populations of rapidly growing cells. The slowly growing bacteria are tolerant of antibiotics and other environmental insults, whereas their isogenic, rapidly growing siblings are sensitive. Recent research has shown that persistence of the model organism Escherichia coli depends on toxin-antitoxin (TA) loci. Deletion of type II TA loci reduces the level of persistence significantly. Lon protease but no other known ATP-dependent proteases is required for persistence. Polyphosphate and (p)ppGpp also are required for persistence. These observations led to the proposal of a simple and testable model that explains the persistence of E. coli. It is now important to challenge this model and to test whether the persistence of pathogenic bacteria also depends on TA loci.
细菌的持续存在是由于在快速生长的细胞群体中存在少数缓慢生长的细菌。缓慢生长的细菌能够耐受抗生素和其他环境胁迫，而它们的同基因、快速生长的同胞则很敏感。最近的研究表明，模型生物大肠杆菌的持续存在取决于毒素-抗毒素（TA）基因座。删除 II 型 TA 基因座会显著降低持续存在的水平。Lon 蛋白酶但不是其他已知的 ATP 依赖性蛋白酶对于持续存在是必需的。聚磷酸盐和 (p)ppGpp 也需要持续存在。这些观察结果导致了一个简单且可测试的模型的提出，该模型解释了大肠杆菌的持续存在。现在重要的是要挑战这个模型，并测试致病性细菌的持续存在是否也依赖于 TA 基因座。
