DNA修复系统中的细菌缺陷可以产生促进适应性微进化的突变菌株。然而,突变菌株在海洋假单胞菌中的作用,能够在生物膜内产生各种功能获得的遗传变异,仍然很大程度上未知。在这项研究中,在脂类假交替单胞菌中mutS的失活使对各种抗生素的耐药性增加了约100倍,包括环丙沙星,利福平和氨基糖苷。此外,溶脂性疟原虫的突变体产生的变体显示出增强的生物膜形成,但降低了游泳运动,表明ΔmutS种群内的表型多样性很高。此外,我们观察到半透明变体的显著生产率约为50%,在生物膜形成中起着重要作用,当ΔmutS菌株在琼脂平板上或在振荡条件下培养时。使用全基因组深度测序结合遗传操作,我们证明了在荚膜生物合成簇内的AT00_17115中的点突变负责在ΔmutS亚群中产生半透明变体,而鞭毛基因fliI和flgP的突变导致游泳运动能力降低。总的来说,这项研究揭示了一种特定的突变驱动的进化,以大量的遗传和表型多样化为特征,从而提供了与微生物适应性相关的遗传属性。
Bacterial deficiencies in the DNA repair system can produce
mutator strains that promote adaptive microevolution. However, the role of
mutator strains in marine Pseudoalteromonas, capable of generating various gain-of-function genetic variants within biofilms, remains largely unknown. In this study, inactivation of mutS in Pseudoalteromonas lipolytica conferred an approximately 100-fold increased resistance to various antibiotics, including ciprofloxacin, rifampicin and aminoglycoside. Furthermore, the
mutator of P. lipolytica generated variants that displayed enhanced biofilm formation but reduced swimming motility, indicating a high phenotypic diversity within the ΔmutS population. Additionally, we observed a significant production rate of approximately 50 % for the translucent variants, which play important roles in biofilm formation, when the ΔmutS strain was cultured on agar plates or under shaking conditions. Using whole-genome deep-sequencing combined with genetic manipulation, we demonstrated that point mutations in AT00_17115 within the capsular biosynthesis cluster were responsible for the generation of translucent variants in the ΔmutS subpopulation, while mutations in flagellar genes fliI and flgP led to a decrease in swimming motility. Collectively, this study reveals a specific
mutator-driven evolution in P. lipolytica, characterized by substantial genetic and phenotypic diversification, thereby offering a reservoir of genetic attributes associated with microbial fitness.