1 ± 1.8% per generation (students t-test p = 0.0002). In animals, 345-2RifC/N3 colonised the pig gut significantly worse than the plasmid Quizartinib solubility dmso free strain or 345-2RifC/R46 (ANOVA F value = 3.41, p = 0.035). In the case of RP1 versus pUB307, these results suggest that the lower fitness cost of pUB307 compared to RP1 is related to the presence of less DNA. It is known that in single copy the Tn1 transposon does not itself have a detrimental effect on host fitness and can occasionally confer a benefit depending on the insertion site [24].

Therefore, it can be assumed that in this case the advantage gained by deletion of Tn1 is due to the presence of less DNA and a lowered burden of gene expression as the TEM beta-lactamase encoded by the transposon is normally expressed at high levels. As RP1 is present in multiple copies, the burden of gene expression will be higher on the plasmid than in the case of Tn1 insertion at a single chromosomal site. Possible additional epistatic fitness effects due to the insertion site GW786034 cost of Tn1 in RP1 will also be absent in pUB307. The reason(s) why N3 and R46 have markedly different fitness costs is less clear, as the two plasmids are a similar size and share the same replication and conjugation functions. The marked fitness difference is therefore most likely due to accessory genes. The antibiotic resistance gene

complement of the two plasmids is similar, although not identical (Figure 1, Table 2). The main differences are the presence of the arsCBADR on R46 and a Type 1 restriction system selleck compound and a number of putative metabolic genes on N3. It is likely that one or more additional genes on N3 are responsible for the high fitness cost of N3 but this hypothesis requires experimental confirmation. Alternatively, a small mutation in the core plasmid genome may also be responsible. The fitness impact of plasmids carrying silent antibiotic resistance genes … In addition to variable fitness costs

brought about by different host-plasmid combinations, bacteria may influence the cost of plasmid carriage by modulation of gene expression. As antibiotic resistance can impose a fitness cost on the bacterial host in the absence of antibiotic selection, one might expect phenotypic silencing of plasmid-borne antibiotic resistance genes to confer a fitness advantage. The fitness costs of the plasmids pVE46 and RP1 on E. coli 345-2RifC had previously been established as moderate in vitro and non-detectable in vivo. Neither plasmid had a detectable cost in the pig gut [26]. However, in both cases isolates that no longer expressed the resistance genes encoded on them but retained intact and wild-type resistance genes, were recovered during the pig gut colonisation experiments [26]. Here, we investigated whether silencing of antibiotic resistance genes carried on pVE46 and RP1 had an effect on their fitness impact.