Microbial biotransformation of trace organic chemicals (TOrCs) is an essential process in wastewater treatment to eliminate environmental pollution. Understanding 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 potential biotransformation drivers concerning functional genes, enzymes, and responsible bacteria. We obtained efficient model communities for completely removing ibuprofen, caffeine, and atenolol, with transformation efficiencies between 0 % and 45 % for sulfamethoxazole, carbamazepine, trimethoprim, and gabapentin. Biotransformation performance was not fully reflected by the presence of known biotransformation genes and enzymes in the metagenomes of the communities. Functional similar homologs to existing biotransformation genes and enzymes (e.g., long-chain-fatty-acid-CoA ligase encoded by fadD and fadD13 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. This study provides fundamental insights into naturally assembled low-complexity degrader communities that can help to identify and tackle the current research gaps on biotransformation.
Keywords: Bioaugmentation; Biodegradation; MAG; Metagenomics; Micropollutants.
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