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TheStaphylococcus aureus global regulator CodY responds to nutrient availability by controlling the expression of target genes.In vitro , CodY represses the transcription of virulence genes, but it is not known if CodY also represses virulencein vivo . The dominant community-associated methicillin-resistantS. aureus (CA-MRSA) clone, USA300, is hypervirulent and has increased transcription of global regulators and virulence genes; these features are reminiscent of a strain defective in CodY. Sequence analysis revealed, however, that thecodY genes of USA300 and other sequencedS. aureus isolates are not significantly different from thecodY genes in strains known to have active CodY.codY was expressed in USA300, as well as in other pulsotypes assessed. Deletion ofcodY from a USA300 clinical isolate resulted in modestly increased expression of the global regulatorsagr andsaeRS , as well as the gene encoding the toxin alpha-hemolysin (hla ). A substantial increase (&gt;30-fold) in expression of thelukF-PV gene, encoding part of the Panton-Valentine leukocidin (PVL), was observed in thecodY mutant. All of these expression differences were reversed by complementation with a functionalcodY gene. Moreover, purified CodY protein bound upstream of thelukSF-PV operon, indicating that CodY directly represses expression oflukSF-PV . Deletion ofcodY increased the virulence of USA300 in necrotizing pneumonia and skin infection. Interestingly, deletion oflukSF-PV from thecodY mutant did not attenuate virulence, indicating that the hypervirulence of thecodY mutant was not explained by overexpression of PVL. These results demonstrate that CodY is active in USA300 and that CodY-mediated repression restrains the virulence of USA300.

CodY Deletion Enhances In Vivo Virulence of Community-Associated Methicillin-Resistant Staphylococcus aureus Clone USA300