Peters J E, Bartoszyk I M, Dheer S, Benson S A
Department of Microbiology, University of Maryland at College Park, 20742, USA.
J Bacteriol. 1996 Jun;178(11):3037-43. doi: 10.1128/jb.178.11.3037-3043.1996.
F plasmids use surface exclusion to prevent the redundant entry of additional F plasmids during active growth of the host cells. This mechanism is relaxed during stationary phase and nonlethal selections, allowing homosexual redundant plasmid transfer. Homosexual redundant transfer occurs in stationary-phase liquid cultures, within nongrowing populations on solid media, and on media lacking a carbon source. We examined the relationship between homosexual redundant transfer, which occurs between F+ hosts, and reversion of a plasmid-encoded lac mutant allele, lacI33omegalacZ. Sodium dodecyl sulfate (SDS) and mutations that prevent normal transfer to F- cells reduced redundant transfer and selection-induced reversion of the lacI33omegalacZ allele. A recA null mutation reduced redundant transfer and selection-induced reversion of the lacI33omegalacZ mutation. Conversely, a recD null mutation increased redundant transfer and selection-induced reversion of the lacI33omegalacZ allele. These results suggest an explanation for why SDS and these mutations affect reversion of the plasmid lacI33omegalacZ allele. However, a direct causal relationship between transfer and reversion remains to be established. These results suggest that Rec proteins play an active role in redundant transfer and/or that redundant transfer is regulated with the activation of recombination. Redundant homosexual plasmid transfer during a period of stress may represent a genetic response that facilitates evolution of plasmid-encoded functions through mutation, recombination, reassortment, and dissemination of genetic elements present in the populations.
F质粒利用表面排斥作用,在宿主细胞活跃生长期间防止额外的F质粒重复进入。在稳定期和非致死性选择期间,这种机制会放松,允许同源性重复质粒转移。同源性重复转移发生在稳定期液体培养物中、固体培养基上的非生长群体内以及缺乏碳源的培养基上。我们研究了发生在F⁺宿主之间的同源性重复转移与质粒编码的乳糖突变等位基因lacI33omegalacZ的回复之间的关系。十二烷基硫酸钠(SDS)以及阻止向F⁻细胞正常转移的突变减少了lacI33omegalacZ等位基因的重复转移和选择诱导的回复。recA基因敲除突变减少了lacI33omegalacZ突变的重复转移和选择诱导的回复。相反,recD基因敲除突变增加了lacI33omegalacZ等位基因的重复转移和选择诱导的回复。这些结果为SDS和这些突变为何影响质粒lacI33omegalacZ等位基因的回复提供了解释。然而,转移和回复之间的直接因果关系仍有待确定。这些结果表明Rec蛋白在重复转移中发挥积极作用和/或重复转移是通过重组激活来调控的。在应激期间的同源性重复质粒转移可能代表一种遗传反应,它通过群体中存在的遗传元件的突变、重组、重配和传播促进质粒编码功能的进化。