Phosphate transport system mediates the resistance of Enterococcus faecalis to multidrug

Enterococcus faecalis, a severe nosocomial and community opportunistic pathogen, is difficult to control due to its multidrug resistance. Through heredity and the recombination of intrinsic resistance genes and horizontally acquired resistance genes, E. faecalis can rapidly evolve drug resistance. N...

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Bibliographic Details
Published in:Microbiological research 2021-08, Vol.249, p.126772-126772, Article 126772
Main Authors: Wei, Lifan, Li, Mingwei, Xia, Feng, Wang, Jia, Ran, Shujun, Huang, Zhengwei, Liang, Jingping
Format: Article
Language:English
Subjects:
Daptomycin
Enterococcus faecalis
Gentamycin
Nisin
Phosphate transport system (PTS)
Transposon insertion sequencing
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Summary:Enterococcus faecalis, a severe nosocomial and community opportunistic pathogen, is difficult to control due to its multidrug resistance. Through heredity and the recombination of intrinsic resistance genes and horizontally acquired resistance genes, E. faecalis can rapidly evolve drug resistance. Nisin, an important antimicrobial peptide, is extensively employed in the healthcare and food industries to inhibit Gram-positive bacteria and may induce the emergence of nisin-resistant bacteria worldwide. However, the mechanism governing nisin resistance in E. faecalis has not been fully elucidated. This study utilizes transposon insertion sequencing (TIS) to comprehensively explore novel genes related to nisin resistance. According to the analysis of TIS results, hundreds of genes appear to be essential for nisin resistance in E. faecalis. The phosphate transport system (OG1RF_10018−10021, named PTS), which is screened by TIS results, enhances the resistance of E. faecalis to nisin, the mechanism of which may be involved in potA and/or OG1RF_10526 (hypothetical gene). Meanwhile, PTS also strongly represses the biosynthesis of ribosomes to increase the sensitivity of E. faecalis to gentamycin. In addition, the overexpression of PTS increases the sensitivity of E. faecalis to daptomycin, the mechanism of which is independent of the LiaFSR system. This study first demonstrated that E. faecalis utilizes PTS to mediate the resistance to multidrug, which may help to elucidate the mechanism governing drug resistance and to establish guidelines for the treatment of infectious diseases caused by E. faecalis.
ISSN:0944-5013
1618-0623
DOI:10.1016/j.micres.2021.126772