Olsen R H
J Bacteriol. 1978 Jan;133(1):210-6. doi: 10.1128/jb.133.1.210-216.1978.
Tn1 transposes from pRO161, a Tra- derivative of RP1, to Pseudomonas aeruginosa sex factor FP2. The acquisition of Tn1 by FP2 results in its ability to mobilize pRO161 to other bacteria. Genetic evidence presented here suggests two sequential mechanisms. Initially, transposition of Tn1 results in trans-diploidy for the Tra+ and Tra- plasmids. This subsequently allows mobilization of the Tra- R-plasmid dependent on a host recombination mechanism. Transconjugants from this mating contain either stable cointegrate R-plasmids or aggregates resulting from dissociation of the cointegrates into a Tra+ and Tra- plasmid. These aggregates have lost at least part of Tn1 from their parent FP2:Tn1 component, but now they mobilize the tra- R-plasmid from a recombination-deficient (Rec-) genetic background as well as from Rec+ donor strains. Transconjugants from these retransfer matings are aggregates. These results suggest a contribution of transposons to R-plasmid evolution and dissemination beyond the mere acquisition of resistance to a given antibiotic.
Tn1从pRO161(RP1的一种Tra-衍生物)转座到铜绿假单胞菌性因子FP2。FP2获得Tn1后使其能够将pRO161转移到其他细菌。本文提供的遗传学证据表明存在两种连续的机制。最初,Tn1的转座导致Tra+和Tra-质粒形成转二倍体。这随后允许依赖宿主重组机制来转移Tra- R质粒。此次交配产生的接合子含有稳定的共整合R质粒或由共整合体解离成Tra+和Tra-质粒而产生的聚集体。这些聚集体已从其亲本FP2:Tn1组分中丢失了至少一部分Tn1,但现在它们能够从重组缺陷(Rec-)遗传背景以及Rec+供体菌株中转移tra- R质粒。这些再次转移交配产生的接合子是聚集体。这些结果表明转座子对R质粒进化和传播的贡献不仅仅是获得对特定抗生素的抗性。