Profiling trace organic chemical biotransformation genes, enzymes and associated bacteria in microbial model communities

Abstract Microbial biotransformation of trace organic chemicals (TOrCs) is an essential process in wastewater treatment for eliminating environmental pollution. Understanding of TOrC biotransformation mechanisms, especially at their original concentrations, is important to optimize treatment performance, whereas our current knowledge is limited. Here we investigated the biotransformation of seven TOrCs by 24 model communities. The genome-centric analyses unraveled the biotransformation drivers concerning functional genes and enzymes and responsible bacteria. We obtained efficient model communities for complete removal on ibuprofen, caffeine and atenolol, and the transformation efficiencies for sulfamethoxazole, carbamazepine, trimethoprim and gabapentin were 0-45%. Biotransformation performance was not fully reflected by the presence of known biotransformation genes and enzymes. However, functional similar homologs to existing biotransformation genes and enzymes (e.g., long-chain-fatty-acid-CoA ligase encoded by fadD and fadD13 gene, acyl-CoA dehydrogenase encoded by fadE12 gene) could play critical roles in TOrC metabolism. Finally, we identified previously undescribed degrading strains, e.g., Rhodococcus qingshengii for caffeine, carbamazepine, sulfamethoxazole and ibuprofen biotransformation, and potential transformation enzymes, e.g., SDR family oxidoreductase targeting sulfamethoxazole and putative hypothetical proteins for caffeine, atenolol and gabapentin biotransformation.