期刊
JOURNAL OF INFECTIOUS DISEASES
卷 205, 期 11, 页码 1677-1687出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jis252
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资金
- National Institute of Allergy and Infectious Diseases
- National Institutes of Health, Department of Health and Human Services [HHSN272200900018C, HHSN266200400001C]
- Australian National Health and Medical Research project grant [APP1008973]
- Australian National Health and Medical Research Council [APP606961]
- Australian Postgraduate Award
The genetic mechanisms that contribute to reduced susceptibility to vancomycin in Staphylococcus aureus are complex and heterogeneous. In addition, debate is emerging as to the true effect of reduced susceptibility to vancomycin on staphylococcal virulence. To investigate this, comparative genomics was performed on a collection of vancomycin-exposed isogenic S. aureus pairs (14 strains in total). Previously described mutations were observed in genes such as vraG, agrA, yvqF, and rpoB; however, a new mechanism was identified involving a serine/threonine phosphatase, Stp1. After constructing an stp1 deletion mutant, we showed that stp1 is important in vancomycin susceptibility and cell wall biosynthesis. Gene expression studies showed that stp1 also regulates virulence genes, including a hemolysin, superantigen-like protein, and phenol-soluble modulin, and that the deletion mutant is attenuated in virulence in vivo. Stp1 provides a new link between vancomycin susceptibility and virulence in S. aureus.
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