Deciphering of sulfonamide biodegradation mechanism in wetland sediments: from microbial community and individual populations to pathway and functional genes.

Figuring out the comprehensive metabolic mechanism of sulfonamide antibiotics (SA) is critical to improve and optimize SA removal in the bioremediation process, but relevant studies are still lacking. Here, an approach integrating metagenomic analysis, degraders' isolation, reverse transcriptional quantification and targeted metabolite determination was used to decipher microbial interactions and functional genes' characteristics in SA-degrading microbial consortia enriched from wetland sediments. The SA-degrading consortia could rapidly catalyze ipso-hydroxylation and subsequent reactions of SA to achieve the complete mineralization of sulfadiazine and partial mineralization of the other two typical SA (sulfamethoxazole and sulfamethazine). Paenarthrobacter, Achromobacter, Pseudomonas and Methylobacterium were identified as the primary participants for the initial transformation of SA. Among them, Methylobacterium could metabolize the heterocyclic intermediate of sulfadiazine (2-aminopyrimidine), and the owning of sadABC genes (SA degradation genes) made Paenarthrobacter have relatively higher SA-degrading activity. Besides, the coexistence of sadABC genes and sul1 gene (SA resistance gene) gave Paenarthrobacter a dual resistance mechanism to SA. The results of reverse transcription quantification further demonstrated that the activity of sadA gene was related to the biodegradation of SA. Additionally, sadABC genes were relatively conserved in a few Microbacteriaceae and Micrococcaceae SA-degraders, but the multiple recombination events caused by densely nested transposase encoding genes resulted in the differential sequence of sadAB genes in Paenarthrobacter genome. These new findings provide valuable information for the selection and construction of engineered microbiomes.