Moxon Richard, Bayliss Chris, Hood Derek
Oxford University Department of Paediatrics, Molecular Infectious Diseases Group, Weatherall Institute of Molecular Medicine Oxford, United Kingdom.
Annu Rev Genet. 2006;40:307-33. doi: 10.1146/annurev.genet.40.110405.090442.
Bacterial pathogens face stringent challenges to their survival because of the many unpredictable, often precipitate, and dynamic changes that occur in the host environment or in the process of transmission from one host to another. Bacterial adaptation to their hosts involves either a mechanism for sensing and responding to external changes or the selection of variants that arise through mutation. Here we review how bacterial pathogens exploit localized hypermutation, through polymerase slippage of simple sequence repeats (SSRs), to generate phenotypic variation and enhanced fitness. These SSRs are located within the reading frame or in the promoter of a subset of genes, often termed contingency loci, whose functions are usually involved in direct interactions with host structures.
由于宿主环境中或从一个宿主传播到另一个宿主的过程中会发生许多不可预测、往往突如其来且动态变化的情况,细菌病原体在生存上面临着严峻挑战。细菌对宿主的适应涉及一种感知和应对外部变化的机制,或者是对通过突变产生的变体的选择。在这里,我们综述了细菌病原体如何通过简单序列重复序列(SSR)的聚合酶滑动利用局部超突变来产生表型变异并提高适应性。这些SSR位于一部分基因的阅读框内或启动子中,这些基因通常被称为应急位点,其功能通常涉及与宿主结构的直接相互作用。