Plasmid encoded fimbriae enforce bacterial interactions
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB14089 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1417840.fastq.gz | Fastqsanger.gz | |||
| ERR1417837.fastq.gz | Fastqsanger.gz | |||
| ERR1417838.fastq.gz | Fastqsanger.gz | |||
| ERR1417839.fastq.gz | Fastqsanger.gz |
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Project description:Conjugative plasmids are the main vehicle for the horizontal spread of antimicrobial resistance (AMR). Although AMR plasmids provide advantages to their hosts under antibiotic pressure, they can also disrupt the cell’s regulatory network, impacting the fitness of their hosts. Despite the importance of plasmid-bacteria interactions on the evolution of AMR, the effects of plasmid carriage on host physiology has remained underexplored, and most studies have focused on model bacteria and plasmids that lack clinical relevance. Here, we analyzed the transcriptional response of 11 clinical enterobacterial strains (2 Escherichia coli, 1 Citrobacter freundii and 8 Klebsiella spp.) and the laboratory-adapted E. coli MG1655 to carriage of pOXA-48, one of the most widely spread carbapenem-resistance plasmids. Our analyses revealed that pOXA-48 produces variable responses on their hosts, but commonly affects processes related to metabolism, transport, response to stimulus, cellular organization and motility. More notably, the presence of pOXA-48 caused an increase in the expression of a small chromosomal operon of unknown function in Klebsiella spp. and C. freundii, which is not present in E. coli. Phylogenetic analysis suggested that this operon has been horizontally mobilized across different Proteobacteria species. We demonstrate that a pOXA-48-encoded LysR transcriptional regulator controls the expression of the operon in Klebsiella spp. and C. freundii. In summary, our results highlight a crosstalk between pOXA-48 and the chromosome of its natural hosts.
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Project description:The multidrug resistance-encoding plasmids belonging to the IncA/C incompatibility group have recently emerged among Escherichia coli and Salmonella enterica in the United States. These plasmids have a unique genetic structure compared to other enterobacterial plasmid types, a broad host range, and propensity to acquire large numbers of antimicrobial resistance genes via their accessory regions. Using E. coli strain DH5α harboring the prototype IncA/C plasmid pAR060302, we sought to define the baseline transcriptome of IncA/C plasmids under laboratory growth and in the face of selective pressure. The effects of ampicillin, florfenicol or streptomycin exposure were compared to cells left untreated at logarithmic phase using Illumina sequencing (RNA-Seq). Under growth in Luria-Bertani broth lacking antibiotics, much of the backbone of pAR060302 was transcriptionally inactive, including its putative transfer regions. A few plasmid backbone genes of interest were highly transcribed, including genes of a putative toxin-antitoxin system and an H-NS-like transcriptional regulator. In contrast, numerous genes within the accessory regions of pAR060302 were highly transcribed, including the resistance genes floR, blaCMY-2, aadA, and aacA. Antibiotic treatment with ampicillin or streptomycin resulted in no genes being differentially expressed compared to controls lacking antibiotics, suggesting that many of the resistance-associated genes are not differentially expressed due to exposure to these antibiotics. In contrast, florfenicol treatment resulted in the up-regulation of floR and numerous chromosomally encoded genes. Overall, the transcriptome mapping of pAR060302 suggests that it mitigates the fitness costs of carrying resistance-associated genes through global regulation with its transcriptional regulators.
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