Expression Is Associated with Pathogenicity

CapB2 is recognized as a tyrosine kinase and is likely a vital factor in extracellular polysaccharide synthesis in , but its pathogenicity function and regulatory mechanism remain obscure. Here, we demonstrate that CapB2 enhances bacterial virulence in a murine model. Mice infected with the wild type SA75 strain exhibited significantly larger ( < 0.05) skin lesions from days 4 to 7 of infection than those challenged with the mutant strain. The effect on virulence was reverted by restoring the mutation to the wild type. The related components of the wild type SA75 cell wall in the mutant strain (SA75Δ) were thinner than wild type SA75 strain and the mutant complemented strain (SA75Δ-C), which was determined by the transmission electron microscopy. The survival percentages of the wild type strain SA75 and SA75Δ-C were significantly higher relative to SA75Δ. The results of qRT-PCR studies also indicated that mutations in regulatory gene led to a drastic increase in capB2 gene transcription, with a 326-fold increase of growth at 6 h compared with the wild type strain, suggesting that sarA is a major negative regulator of capB2 expression. Taken together, these results demonstrate that the expression of CapB2 promotes virulence in a mouse model of skin infection, and that gene transcription is regulated negatively by SarA.