SOS involvement in stress-inducible biofilm formation

Abstract

Bacterial biofilm formation can be induced by antimicrobial and DNA damage agents. These agents trigger the SOS response, in which SOS sensor RecA stimulates auto-cleavage of repressor LexA. These observations lead to a hypothesis of a connection between stress-inducible biofilm formation and the RecA-LexA interplay. To test this hypothesis, three biofilm assays were conducted, viz. the standard 96-well assay, confocal laser scanning microscopy, and the newly developed biofilm-on-paper assay. It was found that biofilm stimulation by the DNA replication inhibitor hydroxyurea was dependent on RecA and appeared repressed by the non-cleavable LexA of Pseudomonas aeruginosa. Surprisingly, deletion of lexA led to reduction of both normal and stress-inducible biofilm formation, suggesting that the wild-type LexA contributes to biofilm formation. The decreases was not the result of poor growth of the mutants. These results suggest SOS involvement in hydroxyurea-inducible biofilm formation. In addition, with the paper biofilm assay, it was found that degradation of the biofilm matrix DNA by DNase I appeared to render the biofilms susceptible to the replication inhibitor. The puzzling questions concerning the roles of LexA in DNA release in the biofilm context are discussed.

Involvement of Stress-Related Genes polB and PA14_46880 in Biofilm Formation of Pseudomonas aeruginosa

“…As a result, these strains become adapted to survive in the stressful niche of CF patient lungs (45). It is likely that replication-inhibiting antibiotics enhance chronic biofilm infections through the SOS response; however, it is possible that SOS response suppression acquired by resistance to DNA-inhibiting antibiotics may also play a role (7,55). Overall, intact SOS and active DNA repair systems seem to be essential for biofilm formation under drug treatment in P. aeruginosa.…”

Adherence to abiotic surface induces SOS response in Escherichia coli K-12 strains under aerobic and anaerobic conditions

“…During SOS, premature cell division is prevented, and genes for DNA damage repair are induced. SulA, the SOS gene product, inhibits cell division by binding to FtsZ to block septum formation until the DNA damage has been repaired (Higashitani et al, 1995;Gotoh et al, 2010). Although the filamentation protects daughter cells from receiving damaged copies of the bacterial chromosome, the filamentous phenotype can also involve other programmes that are designed to promote bacterial survival (Justice et al, 2008).…”

“…Recently, it has been shown that the activation of the SOS response is involved in the adherence to abiotic surfaces by E. coli (Hoffman et al, 2005;Linares et al, 2006;Gotoh et al, 2010), Vibrio cholerae (Hung et al, 2006;Gotoh et al, 2010) and Mycobacterium avium (Geier et al, 2008;Gotoh et al, 2010).…”

“…In the E. coli SOS response, the expression of approximately 40 unlinked genes is induced after the cell is exposed to DNA-damaging agents (Fernández de Henestrosa et al, 2000;Friedberg et al, 2006). Many of these gene products are involved in chromosome recombination, replication, repair, and segregation during cell division (Friedberg et al, 2006;Gotoh et al, 2010). Filamentation is a consequence of the SOS response.…”

The role of bacterial hypermutation in biofilm formation and antibiotic resistance in urinary tract infections caused by pathogens of the Enterobacteriaceae family

“…Several authors have attempted to explain the large amount of hypermutators in a bacterial population known to readily form biofilms. Bacterial biofilm formation can be induced by DNA damaging agents (involved in mutations) triggering the SOS response, through a connection between stress-inducible biofilm formation and the RecA-LexA interplay [49]. Damaging agents have been described, including silver nanoparticles used for their antibacterial properties [50], oxidative product created by other bacteria present in the biofilm (i.e.…”