The novel Pseudomonas aeruginosa two-component regulator BfmR controls bacteriophage-mediated lysis and DNA release during biofilm development through PhdA
Article first published online: 4 JUL 2011
© 2011 Blackwell Publishing Ltd
Volume 81, Issue 3, pages 767–783, August 2011
How to Cite
Petrova, O. E., Schurr, J. R., Schurr, M. J. and Sauer, K. (2011), The novel Pseudomonas aeruginosa two-component regulator BfmR controls bacteriophage-mediated lysis and DNA release during biofilm development through PhdA. Molecular Microbiology, 81: 767–783. doi: 10.1111/j.1365-2958.2011.07733.x
- Issue published online: 24 JUL 2011
- Article first published online: 4 JUL 2011
- Accepted manuscript online: 23 JUN 2011 01:56AM EST
- Accepted 4 June, 2011.
Biofilms are surface-adhered bacterial communities encased in an extracellular matrix composed of polysaccharides, proteins, and extracellular (e)DNA, with eDNA required for biofilm formation and integrity. Here we demonstrate that eDNA release is controlled by BfmR, a regulator essential for Pseudomonas aeruginosa biofilm development. Expression of bfmR coincided with localized cell death and DNA release, and could be stimulated by conditions resulting in membrane perturbation and cell lysis. ΔbfmR mutant biofilms demonstrated increased cell lysis and eDNA release suggesting BfmR to suppress, but not eliminate, these processes. Genome-wide transcriptional profiling indicated that BfmR was required for repression of genes associated with bacteriophage assembly and bacteriophage-mediated lysis. Chromatin immunoprecipitation analysis of direct BfmR targets identified the promoter of PA0691, termed here phdA, encoding a previously undescribed homologue of the prevent-host-death (Phd) family of proteins. Lack of phdA expression coincided with impaired biofilm development and increased cell death, a phenotype comparable to ΔbfmR. Expression of phdA in ΔbfmR restored eDNA release, cell lysis and biofilm formation to wild-type levels, with phdA overexpression promoting resistance to the superinfective bacteriophage Pf4, detected only in biofilms. Therefore, we propose that BfmR regulates biofilm development by limiting bacteriophage-mediated lysis and thus, eDNA release, via PhdA.