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. Author manuscript; available in PMC: 2010 Sep 1.
Published in final edited form as: J Infect Dis. 2009 Sep 1;200(5):724–734. doi: 10.1086/604728

Figure 1.

Figure 1

Mutation in the accessory gene regulator (agr) system of S. aureus in strain LUG855. (A), The agr locus of LUG855. Locations of primers used for allelic replacement with pKOR1 (GBatt1, GBatt2) are shown. The DNA sequence of the intergenic region between the agrBDCA operon and RNAIII is at the bottom, with locations of the P2 and P3 promoters, the corresponding AgrA consensus binding sequences (in boxes), and the site and nature of the mutation observed in LUG855 (up arrow). (B), hemolysis on sheep blood agar plates of streaked cultures. (C), hemolysis of LUG776 and LUG855 in stock cultures showing a homogenous phenotype. (D), δ-toxin expression by RP-HPLC/ESI-MS. Samples were taken from cultures inoculated from pre-cultures and grown for 7 h. (E) EMSA analysis showing dramatic decrease of AgrA binding to the mutated P2 promoter present in LUG855 compared to the original promoter of RN6390 (same sequence as in LUG776 and the other tested strains except LUG855). AgrA concentration was 10 nMol/L. First and second shifts, as previously observed for AgrA binding by Koenig et al. [17], are marked.