These authors contributed equally to this work.
Partially overlapping substrate specificities of staphylococcal group A sortases
Article first published online: 20 SEP 2012
© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Special Issue: Focus on Emerging Gel-Free Separation and Detection Methods
Volume 12, Issue 19-20, pages 3049–3062, October 2012
How to Cite
Sibbald, M. J. J. B., Yang, X.-M., Tsompanidou, E., Qu, D., Hecker, M., Becher, D., Buist, G. and van Dijl, J. M. (2012), Partially overlapping substrate specificities of staphylococcal group A sortases. Proteomics, 12: 3049–3062. doi: 10.1002/pmic.201200144
Colour Online: See the article online to view Fig. 4 in colour.
- Issue published online: 19 OCT 2012
- Article first published online: 20 SEP 2012
- Accepted manuscript online: 28 AUG 2012 11:46AM EST
- Manuscript Accepted: 27 JUL 2012
- Manuscript Revised: 12 JUL 2012
- Manuscript Received: 5 APR 2012
- CEU. Grant Numbers: LSHM-CT-2006–019064, LSHG-CT-2006–037469, PITN-GA-2008–215524
- Scientific Technology Development Foundation of Shanghai. Grant Number: 08JC1401600
- 863 Hi-Tech Program of China. Grant Number: 2006AA02A253
- DFG. Grant Numbers: GK212/3–00, SFB/TR34
- Top Institute Pharma. Grant Number: T4–213
- Staphylococcus aureus;
- Staphylococcus epidermidis
Sortases catalyze the covalent attachment of proteins with a C-terminal LPxTG motif to the cell walls of Gram-positive bacteria. Here, we show that deletion of the srtA genes of Staphylococcus aureus and Staphylococcus epidermidis resulted in the dislocation of several LPxTG proteins from the cell wall to the growth medium. Nevertheless, proteomics and Western blotting analyses revealed that substantial amounts of the identified proteins remained cell wall bound through noncovalent interactions. The protein dislocation phenotypes of srtA mutants of S. aureus and S. epidermidis were reverted by ectopic expression of srtA genes of either species. Interestingly, S. epidermidis contains a second sortase A, which was previously annotated as ``SrtC.'' Ectopic expression of this SrtC in srtA mutant cells reverted the dislocation of some, but not all, cell wall associated proteins. Similarly, defects in biofilm formation were reverted by ectopic expression of SrtC in some, but not all, tested srtA mutant strains. Finally, overexpression of SrtA resulted in increased levels of biofilm formation in some tested strains. Taken together, these findings show that the substrate specificities of SrtA and SrtC overlap partially, and that sortase levels may be limiting for biofilm formation in some staphylococci.