Elucidating the molecular mechanisms underlying nicosulfuron degradation by Serratia sp. NS8 through multi-omics analysis

Nicosulfuron is a widely used sulfonylurea herbicide that generates persistent environmental residues that threaten ecosystems and human health. In this study, an efficient endophytic nicosulfuron-degrading bacterium, Serratia sp. NS8, was isolated from resistant barnyard grass and used to elucidate the molecular basis of nicosulfuron biodegradation. Strain NS8 removed 81.4% of 50 mg·L −1 nicosulfuron within 72 h, and the metabolite profiling revealed multiple degradation routes, including S–N bond cleavage and sulfonylurea bridge hydrolysis. Integrated multi-omics analyses demonstrated that strain NS8 mitigated oxidative injury through the activation of a glutathione-centered antioxidant system, along with the coordinated remodeling of membrane lipids and energy metabolism to generate a synergistic stress-response framework. Disruption of the bssS gene affected both motility and biofilm formation, leading to a corresponding reduction in degradation performance. Moreover, combined gene knockout, complementation, and western blot analyses established atzF as a central functional determinant of nicosulfuron biodegradation, with its deletion causing a 35.55% decline in the degradation efficiency, which was fully restored upon genetic complementation. The subsequent purification of the encoded allophanate hydrolase (AH) yielded a high-purity enzyme that was experimentally confirmed to catalyze the hydrolysis of nicosulfuron to 2-amino-4,6-dimethoxypyridine (ADMP). Collectively, these findings propose a synergistic degradation mechanism in NS8 encompassing antioxidant defense, enzymatic catalysis, and population-level regulatory behaviors, providing both mechanistic insight and a robust microbial candidate for the bioremediation of sulfonylurea herbicide contamination.