DNA repair in bacteria: mechanisms and regulation

Abstract

DNA integrity is important for survival, yet constantly threatened by mutagens, antibiotics, and host defenses. In Escherichia coli, genomic stability is regulated by several repair pathways: direct reversal, base excision repair, nucleotide excision, repair mismatch correction, and homologous recombination coordinated through stress-responsive regulatory networks. Three major regulons exemplify this regulation. The Ada system links direct repair of alkylation damage to transcriptional activation, the Mar system regulates multidrug resistance and oxidative stress tolerance, and the LexA/SOS system orchestrates a global DNA damage response via RecA-mediated LexA cleavage. Together, they show a common concept: repressor-based switches that rapidly convert stress signals into adaptive gene expression. These responses go beyond repair and cause microbes evolution. SOS-induced mutagenesis, while prophage mobilization enhances antibiotic resistance and facilitates horizontal gene transfer, sending virulence factors and influencing infection outcomes. Stress control thereby affects both bacterial survival and host–pathogen dynamics. Insights from E. coli have broader significance. Core repair methods are preserved in eukaryotes, and deficiencies in human processes contribute to genomic instability and cancer. Therapies like PARP inhibitors exploit vulnerabilities in repair, which is like how microbes work. Bacterial stress responses clarify fundamental principles of genome preservation, connecting microbial adaptation with biotechnology, infectious disease biology, and cancer research.