Haines Anthony S, Jones Karen, Batt Sarah M, Kosheleva Irina A, Thomas Christopher M
School of Biosciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Plasmid. 2007 Jul;58(1):76-83. doi: 10.1016/j.plasmid.2007.01.001. Epub 2007 Feb 23.
The antibiotic resistance plasmid pBS228 has been completely sequenced, and revealed to be descended from a plasmid virtually identical to the Birmingham IncP-1alpha plasmid RK2/RP4/RP1. However, it has three additional transposon insertions, one of which is responsible for the extra antibiotic resistances conferred. Loss of kanamycin resistance, which is characteristic of most IncP-1alpha plasmids, is the result of this insertion. A second transposon causes inactivation of the mating pair formation apparatus, rendering the plasmid non-self-transmissible. Comparison with the published data for other IncP-1alpha plasmids gives insight into the recent evolutionary history of this group as well as the acquisition and transmission of one of the first ampicillin resistance transposons discovered.
抗生素抗性质粒pBS228已被完全测序,结果显示它源自一个与伯明翰IncP-1α质粒RK2/RP4/RP1几乎相同的质粒。然而,它有另外三个转座子插入,其中一个导致了额外赋予的抗生素抗性。大多数IncP-1α质粒所特有的卡那霉素抗性丧失就是这种插入的结果。第二个转座子导致交配配对形成装置失活,使该质粒不能自我传递。与其他IncP-1α质粒的已发表数据进行比较,有助于深入了解该群体的近期进化史,以及最早发现的一种氨苄青霉素抗性转座子的获得和传播情况。