Mutations in an organism’s genome can arise spontaneously, that is, in the absence of exogenous stress and prior to selection. Mutations are often neutral or deleterious to individual fitness but can also provide genetic diversity driving evolution. Mutagenesis in bacteria contributes to the already serious and growing problem of antibiotic resistance. However, the negative impacts of spontaneous mutagenesis on human health are not limited to bacterial antibiotic resistance. Spontaneous mutations also underlie tumorigenesis and evolution of drug resistance. To better understand the causes of genetic change and how they may be manipulated in order to curb antibiotic resistance or the development of cancer, we must acquire a mechanistic understanding of the major sources of mutagenesis. Bacterial systems are particularly well-suited to studying mutagenesis because of their fast growth rate and the panoply of available experimental tools, but efforts to understand mutagenic mechanisms can be complicated by the experimental system employed. Here, we review our current understanding of mutagenic mechanisms in bacteria and describe the methods used to study mutagenesis in bacterial systems.

生物体基因组中的突变可以自发产生，即在没有外源压力的情况下并且在选择之前。突变通常对个体适应性是中性的或有害的，但也可以提供驱动进化的遗传多样性。细菌中的诱变助长了已经严重且日益严重的抗生素耐药性问题。但是，自发诱变对人类健康的负面影响不仅限于细菌对抗生素的耐药性。自发突变也是肿瘤发生和耐药性演变的基础。为了更好地了解遗传变化的原因以及如何控制它们以抑制抗生素耐药性或癌症的发展，我们必须对诱变的主要来源有一个机械的理解。由于细菌系统的快速生长速度和可用的实验工具的泛滥，它特别适合研究诱变作用，但是使用诱变的实验系统会使了解诱变机理的工作变得复杂。在这里，我们回顾了我们目前对细菌诱变机理的理解，并描述了用于研究细菌系统诱变的方法。