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The diffusion of KPC-2 carbapenemase is closely related to the spread of  Klebsiella pneumoniae  of the clonal-group 258 and linked to IncFII K  plasmids. Little is known about the biology of multi-drug resistant plasmids and the reasons of their successful dissemination. Using  E. coli  TOP10 strain harboring a multi-replicon IncFII K -IncFIB  bla  KPC−2 -gene carrying plasmid pBIC1a from  K. pneumoniae  ST-258 clinical isolate BIC-1, we aimed to identify basal gene expression and the effects of imipenem exposure using whole transcriptome approach by RNA sequencing (RNA-Seq). Independently of the antibiotic pressure, most of the plasmid-backbone genes were expressed at low levels. The most expressed pBIC1a genes were involved in antibiotic resistance ( bla  KPC−2 ,  bla  TEM  and  aph (3′)-I), in plasmid replication and conjugation, or associated to mobile elements. After antibiotic exposure, 34% of  E. coli  (pBIC1a) genome was differentially expressed. Induction of oxidative stress response was evidenced, with numerous upregulated genes of the  SoxRS/OxyR  oxydative stress regulons, the Fur regulon (for iron uptake machinery), and  IscR  regulon (for iron sulfur cluster synthesis). Nine genes carried by pBIC1a were up-regulated, including the murein DD-endopeptidase  mepM  and the copper resistance operon. Despite the presence of a carbapenemase, we observed a major impact on  E. coli  (pBIC1a) whole transcriptome after imipenem exposure, but no effect on the level of transcription of antimicrobial resistance genes. We describe adaptive responses of  E. coli  to imipenem-induced stress, and identified plasmid-encoded genes that could be involved in resistance to stressful environments.

Transcriptional Landscape of a blaKPC-2 Plasmid and Response to Imipenem Exposure in Escherichia coli TOP10