The Role of the SOS Response in the Adaptation of Pseudomonas aeruginosa

Pseudomonas aeruginosa is a major opportunistic pathogen whose adaptive capacity limits the long-term efficacy of antibiotic therapy. Beyond classical resistance mechanisms, antibiotics may also act as stress signals that alter bacterial physiology and evolutionary trajectories. A central element of this response is the SOS regulatory network, controlled by the RecA–LexA system. Although well studied in Escherichia coli, SOS signaling in P. aeruginosa shows distinct regulatory features that remain incompletely understood. This review summarizes experimental and clinical evidence on antibiotic-induced SOS responses in P. aeruginosa, focusing on fluoroquinolones and other genotoxic agents. Fluoroquinolone exposure consistently induces SOS activation and RecA-dependent signaling, affecting short-term antibiotic susceptibility. However, the available evidence does not support a universal role for SOS activation as a major driver of long-term resistance evolution under most tested conditions. Its relationship with antibiotic-induced mutagenesis remains variable: some studies implicate low-fidelity DNA polymerases, whereas others report mutagenesis independent of canonical RecA–LexA control. Beyond mutagenesis, SOS activation may affect integron dynamics, virulence, and biofilm-associated phenotypes. Overall, in P. aeruginosa, the SOS response appears to be a context-dependent modulator of stress adaptation rather than a universal determinant of resistance evolution.