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.
| Predicate | Object |
|---|---|
| rdf:type | |
| rdfs:comment |
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.
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| skos:exactMatch | |
| uniprot:name |
Plasmid
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| uniprot:author |
Batt S.,
Batt S.M.,
Haines A.S.,
Jones K.,
Kosheleva I.A.,
Thomas C.M.
|
| uniprot:date |
2007
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| uniprot:pages |
76-83
|
| uniprot:title |
Sequence of plasmid pBS228 and reconstruction of the IncP-1alpha phylogeny.
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| uniprot:volume |
58
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| dc-term:identifier |
doi:10.1016/j.plasmid.2007.01.001
|