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Regulation of Staphylococcus aureus α-Toxin Gene (hla) Expression by agr, sarA, and sae in vitro and in Experimental Infective Endocarditis
Yan Q. Xiong, Julie Willard, Michael R. Yeaman, Ambrose L. Cheung and Arnold S. Bayer
The Journal of Infectious Diseases
Vol. 194, No. 9 (Nov. 1, 2006), pp. 1267-1275
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30085924
Page Count: 9
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Background. The Staphylococcus aureus global regulators-agr, sarA, and sae-coordinately control α-toxin gene (hla) expression in vitro. However, their relative in vivo contributions to hla expression, particularly in endovascular infections, have not been defined. Methods. A plasmid-based hla-promoter:green fluorescent protein reporter system was constructed in 2 genetically related S. aureus strains: RN6390 (a natural sigma factor B [sigB]-deficient mutant), SH1000 (a sigB-repaired variant of RN6390 lineage), and their respective agr, sarA, agr/sarA, and sae mutants. These strain sets were used to quantify hla expression in vitro and in an experimental infective endocarditis (IE) model using flow cytometry. Results. In vitro, hla expression was positively modulated by all 3 regulons (sae > agr/sarA > agr and sarA) in both RN6390 and SH1000 backgrounds. In the IE model, hla expression in cardiac vegetations was lower in all single mutants than in the respective parental strains (P<.05 for sae mutant) but was maintained at nearparental levels in the agr/sarA double mutant in both backgrounds. A similar finding was also observed in kidneys and spleens. Conclusions. These results indicate that, although several distinct regulatory circuits can affect hla expression in vitro and in vivo, sae appears to play a crucial role in this context.
The Journal of Infectious Diseases © 2006 Oxford University Press