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TraP is a triply phosphorylated staphylococcal protein that has been hypothesized to be the mediator of a secondStaphylococcus aureus quorum-sensing system, “SQS1,” that controls expression of theagr system and therefore is essential for the organism's virulence. This hypothesis was based on the loss ofagr expression and virulence by atraP mutant of strain 8325-4 and was supported by full complementation of both phenotypic defects by the clonedtraP gene in strain NB8 (Y. Gov, I. Borovok, M. Korem, V. K. Singh, R. K. Jayaswal, B. J. Wilkinson, S. M. Rich, and N. Balaban, J. Biol. Chem. 279:14665-14672, 2004), in which the wild-typetraP gene was expressed intrans in the 8325-4traP mutant. We initiated a study of the mechanism by which TraP activatesagr and found that thetraP mutant strain used for this and other recently published studies has a second mutation, an adventitious stop codon in the middle ofagrA , theagr response regulator. ThetraP mutation, once separated from theagrA defect by outcrossing, had no effect onagr expression or virulence, indicating that theagrA defect accounts fully for the lack ofagr expression and for the loss of virulence attributed to thetraP mutation. In addition, DNA sequencing showed that theagrA gene in strain NB8 (Gov et al., J. Biol. Chem., 2004), in contrast to that in theagr -defective 8325-4traP mutant strain, had the wild-type sequence; further, thetraP mutation in that strain, when outcrossed, also had no effect onagr expression.

infection and immunity

A Nonsense Mutation in agrA Accounts for the Defect in agr Expression and the Avirulence of Staphylococcus aureus 8325-4 traP :: kan