Journal article
Serine/threonine phosphatase stp1 contributes to reduced susceptibility to vancomycin and virulence in staphylococcus aureus
DR Cameron, DV Ward, X Kostoulias, BP Howden, RC Moellering, GM Eliopoulos, AY Peleg
Journal of Infectious Diseases | OXFORD UNIV PRESS INC | Published : 2012
Abstract
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 bi..
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Funding Acknowledgements
This work was supported by the National Institute of Allergy and Infectious Diseases; National Institutes of Health, Department of Health and Human Services (HHSN272200900018C, HHSN266200400001C); and in part by the Australian National Health and Medical Research project grant (APP1008973). We also acknowledge the Australian National Health and Medical Research Council Biomedical Fellowship to A. Y. P. (APP606961) and Australian Postgraduate Award to D. C.