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JAC Advance Access originally published online on September 10, 2008
Journal of Antimicrobial Chemotherapy 2008 62(6):1207-1214; doi:10.1093/jac/dkn363
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Original research

The fusidic acid stimulon of Staphylococcus aureus

Alejandro Delgado1, Shahrear Zaman1, Arunachalam Muthaiyan2, Vijayaraj Nagarajan3, Mohamed O. Elasri3, Brian J. Wilkinson2 and John E. Gustafson1,4,*

1 Microbiology Group, Department of Biology, New Mexico State University, Las Cruces, NM 88003, USA 2 Microbiology Group, Department of Biological Sciences, Illinois State University, Normal, IL 61790, USA 3 Department of Biological Sciences, University of Southern Mississippi, Hattiesburg, MS 39406, USA 4 Molecular Biology Program, New Mexico State University, Las Cruces, NM 88003, USA

Received 23 May 2008; returned 30 June 2008; revised 6 August 2008; accepted 7 August 2008

* Correspondence address. Department of Biology, MSC 3AF, New Mexico State University, PO Box 30001, Las Cruces, NM 88003-8001, USA. Tel: +1-505-646-5660; Fax: +1-505-646-5665; E-mail: jgustafs{at}nmsu.edu

Objectives: Fusidic acid interferes with the release of elongation factor G (EF-G) after the translocation step of protein synthesis. The objective of this study was to characterize the fusidic acid stimulon of a fusidic acid-susceptible strain of Staphylococcus aureus (SH1000).

Methods: S. aureus microarrays and real-time PCR determined transcriptome alterations occurring in SH1000 grown with fusidic acid. The Staphylococcus aureus microarray meta-database (SAMMD) compared and contrasted the SH1000 fusidic stimulon with 89 other S. aureus transcriptional datasets. Fusidic acid gradient analyses with mutant-parent strain pairs were used to identify genes required for intrinsic fusidic acid susceptibility identified during transcriptional analysis.

Results: Many genes altered by fusidic acid challenge are associated with protein synthesis. SAMMD analysis determined that the fusidic acid stimulon has the greatest overlap with the S. aureus cold shock and stringent responses. Six out of nine peptidoglycan hydrolase genes making up the two component YycFG regulon were also up-regulated by fusidic acid, as were a carboxylesterase gene (est) and two putative drug efflux pump genes (emr-qac1 and macA). Genes down-regulated by fusidic acid induction encoded a putative secreted acid phosphatase and a number of protease genes. Roles for the agr operon, the peptidoglycan hydrolase gene isaA and two proteases (htrA1 and htrA2) in the expression of fusidic acid susceptibility were revealed.

Conclusions: The SH1000 fusidic acid stimulon includes genes involved with two stress responses, YycFG-regulated cell wall metabolism, drug efflux, and protein synthesis and turnover.

Keywords: transcriptomics , qacA efflux , carboxypeptidase , yycFG , staphylococcal secretory antigen


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