**7. Conclusions**

Given the mounting threat posed by antibiotic resistance, a better understanding of the mechanisms bacteria employ to evolve resistance, persistence as well as pathogenesis is urgently needed. Conditions conducive to SOS induction are encountered by *E. coli* at various host anatomical sites and drive bacterial adaptation to stress, including antibiotic resistance and amplified toxin production. Numerous interdependent mechanisms involving the SOS response are evident, including amplification of the inducing signal in the bacterial population, e.g. (i) SOS induction of horizontal gene transfer which in turn, via ssDNA transfer, induces the SOS response in recipients, (ii) promotion of biofilm formation that generates a dynamic environment with DNA damaging agents and high cell density, conducive to HGT, all in turn inducing the SOS response, (iii) induction of bacteriocins targeting DNA which induce the SOS response in sensitve cells. Nevertheless, our understnding of the modes and the levels of the SOS response, including its connections with other stress response pathways is still lacking. Novel antimicrobial treatment approaches should seek to target the SOS response, possibly the inducer RecA.

### **Acknowledgements**

This work was funded by grant P1-0198 from the Slovene Research Agency.

### **Conflict of interest**

The authors declare no conflict of interest.

Escherichia coli *- Old and New Insights*
