Far-UVC (222 nm) Suppresses Bacterial UV Resistance and Repair through Inhibition of DNA Repair Pathways

Controlling pathogenic bacteria is essential for safe drinking water, but conventional UV disinfection can be compromised by bacterial DNA repair and radiation-resistant strains. This study demonstrates that microbial radiation resistance is fundamentally wavelength-dependent, established through a molecular-level understanding of DNA repair disruption. While conventional 254 nm UV (UV₂₅₄) and far-UVC 222 nm (UV₂₂₂) induce comparable DNA damage at practical fluences (20-50 mJ/cm² ), UV₂₂₂ uniquely suppresses repair through wavelength-specific protein targeting and damage. UV₂₂₂ enhances protein absorption by 2.58-fold and amino acid photolysis quantum yield and then directly photolyzes substitute repair enzymes, leading to protein fragmentation with almost complete enzymatic inactivation (>95%) compared to UV₂₅₄. This targeted proteome damage systematically dismantles repair pathways, with recA, the master regulator of DNA repair, experiencing >90% transcriptional suppression under UV₂₂₂, contrasting with significantly elevated expression under UV₂₅₄. Genetic validation using recA-deficient mutants confirms this pathway-specific vulnerability. UV₂₂₂-induced protein damage likely mediates inhibition of DNA repair, preventing genomic restoration. This repair suppression mechanism enables UV₂₂₂ to overcome UV₂₅₄-resistant bacteria such as Deinococcus radiodurans and produces multitime scale disinfection in tap water, achieving both immediate inactivation and regrowth prevention. These findings advance understanding of wavelength-dependent UV resistance and bacterial DNA repair processes, providing new insights for improved UV disinfection methods.