Understanding LexA as a central regulator of the bacterial SOS response

The bacterial SOS response is an adaptive mechanism that acts as a final safeguard to ensure survival under genotoxic stress. It can be activated by multiple factors and represents one of the key pathways for stress adaptation, mutagenesis, and survival. For decades, research has focused on deciphering the roles of the master regulators governing this pathway, given their central importance in managing cellular responses to DNA damage. The operational mechanism of the SOS response has also been extensively studied. Numerous genes participate in this network, displaying diversity in their regulation. In addition to the SOS pathway, bacteria employ other damage-inducible systems for stress tolerance and survival, several of which have recently been explored. LexA, a key regulator of the SOS response, exhibits additional moonlighting roles and has gained attention as a promising anti-mutagenic target owing to its absence in mammalian systems. With the growing challenge of drug resistance, such alternative strategies could effectively complement traditional antimicrobial approaches. This review underscores these critical aspects to inspire further research and scientific advancement.