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Mutation of  sarA  in  Staphylococcus aureus  results in a reduced capacity to form a biofilm, but the mechanistic basis for this remains unknown. Previous transcriptional profiling experiments identified a number of genes that are differentially expressed both in a biofilm and in a  sarA  mutant. This included genes involved in acid tolerance and the production of nucleolytic and proteolytic exoenzymes. Based on this we generated mutations in  alsSD ,  nuc  and  sspA  in the  S. aureus  clinical isolate UAMS-1 and its isogenic  sarA  mutant and assessed the impact on biofilm formation. Because expression of  alsSD  was increased in a biofilm but decreased in a  sarA  mutant, we also generated a plasmid construct that allowed expression of  alsSD  in a  sarA  mutant. Mutation of  alsSD  limited biofilm formation, but not to the degree observed with the corresponding  sarA  mutant, and restoration of  alsSD  expression did not restore the ability to form a biofilm. In contrast, concomitant mutation of  sarA  and  nuc  significantly enhanced biofilm formation by comparison to the  sarA  mutant. Although mutation of  sspA  had no significant impact on the ability of a  sarA  mutant to form a biofilm, a combination of protease inhibitors (E-64, 1-10-phenanthroline, and dichloroisocoumarin) that was shown to inhibit the production of multiple extracellular proteases without inhibiting growth was also shown to enhance the ability of a  sarA  mutant to form a biofilm. This effect was evident only when all three inhibitors were used concurrently. This suggests that the reduced capacity of a  sarA  mutant to form a biofilm involves extracellular proteases of all three classes (serine, cysteine and metalloproteases). Inclusion of protease inhibitors also enhanced biofilm formation in a  sarA/nuc  mutant, with the combined effect of mutating  nuc  and adding protease inhibitors resulting in a level of biofilm formation with the  sarA  mutant that approached that of the UAMS-1 parent strain. These results demonstrate that the inability of a  sarA  mutant to repress production of extracellular nuclease and multiple proteases have independent but cumulative effects that make a significant contribution to the biofilm-deficient phenotype of an  S. aureus sarA  mutant.

Factors Contributing to the Biofilm-Deficient Phenotype of Staphylococcus aureus sarA Mutants