Antibiotic concentrations RNA extraction.

<div> Bacteria can quickly adapt to sub-lethal concentrations of antibiotics. Several stress and DNA repair genes contribute to this adaptation process. However, the pathways leading to adaptation by acquisition of <i>de novo</i> mutations remain poorly understood. This study explored the roles of DNA polymerase IV (<i>dinB</i>) and catalase HP2 (<i>katE</i>) in <i>E</i>. <i>coli</i>’s adaptation to amoxicillin. These genes are thought to play essential roles in beta-lactam resistance—<i>dinB</i> in increasing mutation rates and <i>katE</i> in managing oxidative stress. By comparing the adaptation rates, transcriptomic profiles, and genetic changes of wild-type and knockout strains, we aimed to clarify the contributions of these genes to beta-lactam resistance. While all strains exhibited similar adaptation rates and mutations in the <i>frdD</i> gene and <i>ampC</i> operon, several unique mutations were acquired in the Δ<i>katE</i> and Δ<i>dinB</i> strains. Overall, this study distinguishes the contributions of general stress-related genes on the one hand, and <i>dinB</i>, and <i>katE</i> on the other hand, in development of beta-lactam resistance. </div>