A point mutation in the agr locus caused previously reported phenotypes in Staphylococcus aureus pneumonia

ABSTRACT: The role of Pantonâ??Valentine leukocidin (PVL) in Staphylococcus aureus pathogenesis is controversial. Here, we show that an unintended point mutation in the agr P2 promoter of S.aureus caused the phenotypes in gene regulation and murine pneumonia attributed to PVL by Labandeiraâ??Rey et al. (Science 315:1130â??3, 2007). In agreement with previous studies that failed to detect similar effects of PVL using communityâ??associated methicillinâ??resistant S. aureus strains, we found no significant impact of PVL on gene expression or pathogenesis after we repaired the mutation. These findings further contribute to the idea that PVL does not have a major impact on S. aureus pathogenesis and resolve debate about its role in murine infection models. Moreover, our results demonstrate that a single

ORGANISM(S): Staphylococcus aureus

SUBMITTER: Amer Villaruz 

PROVIDER: E-GEOD-14394 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress