Abstract
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.
Original language | English |
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Pages (from-to) | 76-83 |
Number of pages | 8 |
Journal | Plasmid |
Volume | 58 |
Issue number | 1 |
DOIs | |
Publication status | Published - 1 Jul 2007 |
Keywords
- transposable element
- antibiotic resistance
- broad host range
- ampicillin resistance
- evolution
- Tn1