Phenotypic and genetic heterogeneities are conserved features of prokaryotic populations. During periods of stress, this programmed diversity increases the likelihood that variants within the population will survive the adverse conditions, allowing for proliferation. Phenotypic heterogeneity can have a mutational or indeed a non-mutational basis as observed in bet-hedging strategies adopted by antibiotic-tolerant persister cells. Genetic variants can arise by phase variation (slip-strand mispairing, promoter inversions etc.), nucleotide polymorphisms resulting from replication errors or larger rearrangements such as deletions and insertions. In the face of selective pressures, these alterations may be neutral, beneficial or deleterious.

We recently described the genetic basis of tolerance to a normally toxic metabolite, d-serine (d-ser) in enterohaemorrhagic E. coli (EHEC). Here we summarize our work in the context of population dynamics, provide further discussion on the distinction between these tolerance mechanisms and the importance of heterogeneity for maximising adaptive potential.

表型和遗传异质性是原核种群的保守特征。在压力时期，这种程序化的多样性增加了种群中的变异在不利条件下存活的可能性，从而允许增殖。表型异质性可以具有突变或实际上非突变的基础，正如在抗生素耐受性持久细胞采用的对冲策略中所观察到的那样。遗传变异可能由相位变异（滑链错配、启动子倒位等）、复制错误或更大的重排（如缺失和插入）导致的核苷酸多态性产生。面对选择压力，这些改变可能是中性的、有益的或有害的。

我们最近描述了对肠出血性大肠杆菌(EHEC) 中通常有毒的代谢物d-丝氨酸 ( d- ser)耐受的遗传基础。在这里，我们总结了我们在种群动态背景下的工作，进一步讨论了这些耐受机制之间的区别以及异质性对于最大化适应潜力的重要性。