Abstract
Plasmids play a crucial role in spreading antimicrobial resistance genes. Plasmids have many ways to incorporate various genes. By inducing amoxicillin resistance in Escherichia coli, followed by horizontal gene transfer experiments and sequencing, we show that the chromosomal beta-lactamase gene ampC is multiplied and results in an 8–13 kb contig. This contig is comparable to a transposon, showing similarities to variable regions found in environmental plasmids, and can be transferred between E. coli cells. As in eight out of nine replicate strains an almost completely identical transposon was isolated, we conclude that this process is under strict control by the cell. The single transposon that differed was shortened at both ends, but otherwise identical. The outcome of this study indicates that as a result of exposure to beta-lactam antibiotics, E. coli can form a transposon containing ampC that can subsequently be integrated into plasmids or genomes. This observation offers an explanation for the large diversity of genes in plasmids found in nature and proposes mechanisms by which the dynamics of plasmids are maintained.
Highlights
Plasmids have a crucial role in spreading genes coding for antimicrobial resistance, and a large variety of resistance plasmids has been described in considerable detail [1,2]
What are the driving factors causing the genesis of plasmids and their subsequent spreading? That a microbe carrying a plasmid coding for resistance against a certain antibiotic will have a selective advantage when exposed to that compound is obvious, but where did that plasmid originate from in the first place? The chromosomal ampC gene of Escherichia coli codes for a beta-lactamase but is normally expressed at very low levels
The outcome of this study shows that resistance can be induced by exposure to the beta-lactam antibiotic amoxicillin in E. coli by multiplication and mutation of the chromosomal ampC gene
Summary
Plasmids have a crucial role in spreading genes coding for antimicrobial resistance, and a large variety of resistance plasmids has been described in considerable detail [1,2].In contrast, the ontogeny of resistance plasmids is not well understood. Plasmids have a crucial role in spreading genes coding for antimicrobial resistance, and a large variety of resistance plasmids has been described in considerable detail [1,2]. That a microbe carrying a plasmid coding for resistance against a certain antibiotic will have a selective advantage when exposed to that compound is obvious, but where did that plasmid originate from in the first place? Mutations in the promoter region induced by exposure to beta-lactam antibiotics cause overexpression, which results in resistance to certain beta-lactam antibiotics, such as amoxicillin. This gene is multiplied between 20 to 600 times when E. coli is made resistant to amoxicillin by exposure to stepwise increasing concentrations [3]. This study addresses the question whether the multiple copies of the ampC gene can form a transposon that could possibly be transferred to other E. coli cells
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