Journal
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
Volume 65, Issue 4, Pages -Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/AAC.02229-20
Keywords
plasmids; mobile genetic elements; Pseudomonas spp.; site-specific integrase; efflux pumps; Enterobacteriaceae
Categories
Funding
- National Natural Science Foundation of China [31625026, 32002338]
- Guangdong Special Support Program Innovation Team [2019BT02N054]
- 111 Project [D20008]
- Innovation Team Project of Guangdong University [2019KCXTD001]
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The study identified a novel mobile gene cluster, tmexCD2-toprJ2, present in Raoultella ornithinolytica, which confers resistance to multiple antimicrobials and may have originated from a Pseudomonas species. The expression of tmexCD2-toprJ2 in Escherichia coli resulted in increased resistance to tigecycline and decreased susceptibility to other antimicrobials. Genetic context analyses demonstrated that tmexCD2-toprJ2 might have been captured and mobilized by a XerD-like tyrosine recombinase system.
We recently identified a novel plasmid-mediated resistance-nodulationdivision (RND)-type efflux pump gene cluster, tmexCD1-toprJ1, in Klebsiella pneumoniae that conferred resistance to multiple antimicrobials, including tigecycline. While homologs of tmexCD1-toprJ1 were found encoded in many other bacterial species in GenBank, their functions and transfer mechanisms remain unknown. This study identified another mobile gene cluster, tmexCD2-toprJ2, co-occurring on both a plasmid (pHNNC189-2) and the chromosome of a clinical Raoultella ornithinolytica isolate, strain NC189, producing KPC-2, NDM-1, and RmtC. tmexCD2-toprJ2 shares high similarity at the nucleotide level with tmexCD1-toprJ1, with 98.02%, 96.75%, and 99.93% identities to tmexC1, tmexD1, and toprJ1, respectively. Phylogenetic analysis revealed that tmexCD2-toprJ2 may have originated from the chromosome of a Pseudomonas species. The expression of tmexCD2-toprJ2 in an Escherichia coli strain resulted in an 8-fold increase in the tigecycline MIC and decreased susceptibility to other antimicrobials. Genetic context analyses demonstrated that tmexCD2-toprJ2, together with the adjacent hypothetical site-specific integrase genes, was possibly captured and mobilized by a XerD-like tyrosine recombinase system, forming a putative transposition unit (xerD-like-int3-like-thf2-ybjD-umuD-Delta umuC1-int1-like-im2-like-hp1-hp2-tnfxB2-ISBvi2-tmexCD2-toprJ2-Delta umuC1), which was inserted into umuC-like genes in both the NC189 plasmid pHNNC189-2 and the chromosome. Since tmexCD1-toprJ1 and tmexCD2-toprJ2 could confer multidrug resistance, the spread of these gene clusters, associated with the new recombinase system, calls for more attention.
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