Skip to main content
Fig. 6 | Annals of Clinical Microbiology and Antimicrobials

Fig. 6

From: Genomic insights into the evolution and mechanisms of carbapenem-resistant hypervirulent Klebsiella pneumoniae co-harboring blaKPC and blaNDM: implications for public health threat mitigation

Fig. 6

Genetic structures of the conjugative hybrid resistance plasmid fusion regions. A Alignment of hybrid resistance plasmids pJ-JNKPN26-1-NDM, pJ-JNKPN26-2_HNK, pJ-JNKPN26-3_HNK, and pJ-JNKPN26-4_HNK with parental plasmids from JNKPN26. Black, yellow, red, cyan-blue, and other colored arrows indicate other function protein, conjugation transfer, resistance gene, IS insertion site, and mobile element protein, respectively. The evidence for the occurrence of the fusion event in transconjugant J-JNKPN261-1 was the emergence of TnAs1 on pJ-JNKPN26-1-NDM. C The resistance genes are indicated by rectangles. A target site and subsequent 8-bp duplications are indicated by a vertical flag. The relative frequencies of IS26- and TnAs1-mediated reactions are indicated by blue and green arrows, respectively. Proposed mechanisms of plasmid fusion. i pJ-JNKPN26-1_NDM and pJNKPN26-2_HNK: TnAs1 attacked the dnaQ gene of pJNKPN26-NDM, leading to the formation of fusion plasmids through a replicative transposition mechanism. ii pJ-JNKPN26-3_HNK: TnAs1 interrupted the uvrD gene of pJNKPN26-NDM, leading to the reverse insertion of pJNKPN26-KPC into pJ-JNKPN26-1-NDM forming plasmid pJ-JNKPN26-3_HNK. iii pJ-JNKPN26-4_HNK: formation of cointegration was mediated by IS26 interrupting ISEcp1

Back to article page