spxA1-null mutant of Streptococcus sanguinis SK36

Transcriptional profiling of the spxA1-null mutant of Streptococcus sanguinis SK36 compared with wild type. The spxA1 gene was inactivated in Streptococcus sanguinis SK36, and the mutant demonstrated opaque colony morphology, reduced hydrogen peroxide (H2O2) production, and reduced antagonistic activity against Streptococcus S. mutans UA159 both on plates and in liquid media. The mutant also showed decreased tolerance to high temperature, and acidic and oxidative stresses. Complementation of the ΔspxA1 mutant with spxA1 restored colony morphology, H2O2 production and stress tolerance to the ΔspxA1 mutant. The mutant also exhibited an ~5-fold reduction in competitiveness in an animal model of endocarditis, indicating the involvement of SpxA1 in endocarditis virulence. Microarray studies revealed that a number of SpxA1-upregulated genes are involved in oxidative stress. The expression of spxB and nox (which encode pyruvate oxidase and NADH oxidase, respectively, and are involved in H2O2 production and nox involved virulence) significantly decreased in ΔspxA1 compared with the wild type. This may be at least partly responsible for the decreased H2O2 production and reduced virulence in the ΔspxA1 mutant because spxB and nox were involved in H2O2 production and nox involved virulence. One-condition experiment: ΔspxA1 vs. S. sanguinis SK36 cells. Biological replicates: 3 wild type, 3 ΔspxA1, independently grown and harvested. One replicate (one wild type and one ΔspxA1 mixture) per array.