Abstract

Antimicrobial resistance poses a major threat to public health. An alternative treatment is the use of bacteriophages. Prokaryotes have multiple resistance mechanisms against bacteriophage infection. These include the adaptive immune system CRISPR Cas. To produce immunity, ~ 30 bp DNA segments are integrated into CRISPR arrays as unique spacer sequences. I demonstrate that the activation of the SOS response aids in spacer acquisition. The catalytic activity of Cas1-Cas2 results in cellular filamentation due to the induction of sulA. Furthermore, the use of the lexA3 allele, which prevents the induction of the SOS response and consequent sulA expression, reduces the rate of adaptation. In summary, preventing the induction of the SOS response will reduce the acquisition of novel spacers to increase the efficiency of bacteriophage therapy.