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

Abstract

During the colonization of surfaces, Escherichia coli bacteria often encounter DNA-damaging agents and these agents can induce several defence mechanisms. Base excision repair (BER) is dedicated to the repair of oxidative DNA damage caused by reactive oxygen species (ROS) generated by chemical and physical agents or by metabolism. In this work, we have evaluated whether the interaction with an abiotic surface by mutants derived from E. coli K-12 deficient in some enzymes that are part of BER causes DNA damage and associated filamentation. Moreover, we studied the role of endonuclease V (nfi gene; 1506 mutant strain) in biofilm formation. Endonuclease V is an enzyme that is involved in DNA repair of nitrosative lesions. We verified that endonuclease V is involved in biofilm formation. Our results showed more filamentation in the xthA mutant (BW9091) and triple xthA nfo nth mutant (BW535) than in the wild-type strain (AB1157). By contrast, the mutant nfi did not present filamentation in biofilm, although its wild-type strain (1466) showed rare filaments in biofilm. The filamentation of bacterial cells attaching to a surface was a consequence of SOS induction measured by the SOS chromotest. However, biofilm formation depended on the ability of the bacteria to induce the SOS response since the mutant lexA Ind " did not induce the SOS response and did not form any biofilm. Oxygen tension was an important factor for the interaction of the BER mutants, since these mutants exhibited decreased quantitative adherence under anaerobic conditions. However, our results showed that the presence or absence of oxygen did not affect the viability of BW9091 and BW535 strains. The nfi mutant and its wild-type did not exhibit decreased biofilm formation under anaerobic conditions. Scanning electron microscopy was also performed on the E. coli K-12 strains that had adhered to the glass, and we observed the presence of a structure similar to an extracellular matrix that depended on the oxygen tension. In conclusion, it was proven that bacterial interaction with abiotic surfaces can lead to SOS induction and associated filamentation. Moreover, we verified that endonuclease V is involved in biofilm formation.

Global gene expression in Escherichia coli, isolated from the diseased ocular surface of the human eye with a potential to form biofilm

“…Concomitantly, in the present study yhj N coding for cellulose synthase regulator protein was up regulated where as in ABU strains of E. coli genes involved in cellulose synthesis ( bcs ABZC and bcs EFGgenes) were down regulated [43]. Genes encoding colanic acid synthesis ( wca L and wca M) were down regulated in the ocular E. coli and ABU strains [43] probably because expression of colanic acid inhibits the biofilm ability of E. coli [57]. Further in ocular E. coli L-1216/2010 colicin protecting conserved protein encoding genes cbr B and cbr C are up regulated by 11- and 288-folds respectively compared to the non-biofilm forming cells.…”

Quinolone Resistance Reversion by Targeting the SOS Response

“…The SOS pathway is initiated through the activation of RecA, which in turn induces autocatalytic cleavage of the LexA repressor and induces the SOS response genes ( 8 , 10 ). RecA is involved in DNA repair, recombination, induction of the SOS response, horizontal gene transfer, and biofilm formation ( 10 , 12 – 14 ). Systematically altering bacterial SOS activity, both constitutive SOS activation and inactivation, has been revealed as a therapeutic strategy for potentiating bactericidal antibiotics like quinolones against highly susceptible wild-type E. coli ( 15 , 16 ).…”

Modulation of Bacterial Proliferation as a Survival Strategy

“…Interestingly, UPEC cells did not filament in host cells defective for pathogen recognition suggesting that filamentation is a regulated response to an active innate host response. It has also been observed that E. coli forms filaments when adhering to certain abiotic surfaces, which was proposed to be a result of DNA damage, possibly caused by damaging agents present on the surface (Costa et al, 2014). It is also well known that antibiotics induce cell filamentation.…”