Biofilms are communities of microorganisms attached to a surface or each other. Biofilm-associated cells are the etiologic agents of recurrent Staphylococcus aureus infections. Infected human tissues are hypoxic or anoxic. S. aureus increases biofilm formation in response to hypoxia, but how this occurs is unknown. In the current study we report that oxygen influences biofilm formation in its capacity as a terminal electron acceptor for cellular respiration. Genetic, physiological, or chemical inhibition of respiratory processes elicited increased biofilm formation. Impaired respiration led to increased cell lysis via divergent regulation of two processes: increased expression of the AtlA murein hydrolase and decreased expression of wall-teichoic acids. The AltAdependent release of cytosolic DNA contributed to increased biofilm formation. Further, cell lysis and biofilm formation were governed by the SrrAB two-component regulatory system. Data presented support a model wherein SrrAB-dependent biofilm formation occurs in response to the accumulation of reduced menaquinone. The Boyd lab is supported by Rutgers University, the Charles and Johanna Busch foundation and USDA MRF project NE-1028. AAM is supported by the Douglas Eveleigh fellowship from the Microbial Biology Graduate Program and an Excellence Fellowship from Rutgers University. The authors would like to thank Dr. William Belden for use of his real-time thermocycler. We thank Dr. Jeffrey Bose and Dr. Kenneth Bayles for kindly sharing the atlA plasmids and strains with us. We thank Dr. Alex Horswill and Dr. Ann Stock for sharing S. aureus clinical isolates.
All Science Journal Classification (ASJC) codes
- Immunology and Microbiology(all)
- Biochemistry, Genetics and Molecular Biology(all)