Effects of a putative staphylococcus aureus two-component regulatory system on srtA transcription and biofilm formation

Abstract

Staphylococcus aureus bacteria have evolved mechanisms to block the effects of antibiotics. After treatment for methicillin-resistant S. aureus (MRSA) infections, persister cells develop that have the ability to survive but not grow in the presence of the drug. Not a lot is known about persister cells, so it is important to study the mechanism for their ability to persist in the presence of antibiotics. Our proposed mechanism for persister formation in S. aureus is the ability of a drug or environmental stressor to impact gene regulation by a two-component regulatory system that affects transcription of the sortase A gene srtA. In this study, we have looked at the effects of the drug SK-03-92 on biofilm formation by down-regulating a putative two-component regulatory system. To determine how the tow-component system impacts srtA transcription and biofilm formation, strains were obtained with mutations in either the response regulator or the sensor kinase gene. Overall biofilm formation, srtA transcription, and primary attachment were increased in the sensor kinase mutant strain, while the response regulator mutant strain results were similar to that of the wild-type strain. Overall, the data demonstrated that a mutation in the hypothesized sensor kinase resulted in a 10-fold increase in srtA transcription.