Bisphenol A (BPA) pollution poses an increasingly serious problem. BPA has been detected in a variety of environmental media and human tissues. Microbial degradation is an effective method of environmental BPA remediation. However, BPA is also biotoxic to microorganisms. In this study, Rhodococcus equi DSSKP-R-001 (R-001) was used to degrade BPA, and the effects of BPA on the growth metabolism, gene expression patterns, and toxicity-resistance mechanisms of Rhodococcus equi were analyzed. The results showed that R-001 degraded 51.2% of 5 mg/L BPA and that 40 mg/L BPA was the maximum BPA concentration tolerated by strain R-001. Cytochrome P450 monooxygenase and multicopper oxidases played key roles in BPA degradation. However, BPA was toxic to strain R-001, exhibiting nonlinear inhibitory effects on the growth and metabolism of this bacterium. R-001 bacterial biomass, total protein content, and ATP content exhibited V-shaped trends as BPA concentration increased. The toxic effects of BPA included the downregulation of R-001 genes related to glycolysis/gluconeogenesis, pentose phosphate metabolism, and glyoxylate and dicarboxylate metabolism. Genes involved in aspects of the BPA-resistance response, such as base excision repair, osmoprotectant transport, iron-complex transport, and some energy metabolisms, were upregulated to mitigate the loss of energy associated with BPA exposure. This study helped to clarify the bacterial mechanisms involved in BPA biodegradation and toxicity resistance, and our results provide a theoretical basis for the application of strain R-001 in BPA pollution treatments.

Estrogen contamination is recognized as one of the most serious environmental problems, causing widespread concern worldwide. Environmental estrogens are mainly derived from human and vertebrate excretion, drugs, and agricultural activities. The use of microorganisms is currently the most economical and effective method for biodegradation of environmental estrogens. Rhodococcus equi DSSKP-R-001 (R-001) has strong estrogen-degrading capabilities. Our study indicated that R-001 can use different types of estrogen as its sole carbon source for growth and metabolism, with final degradation rates above 90%. Transcriptome analysis showed that 720 (E1), 983 (E2), and 845 (EE2) genes were significantly upregulated in the estrogen-treated group compared with the control group, and 270 differentially expressed genes (DEGs) were upregulated across all treatment groups. These DEGs included ABC transporters; estrogen-degrading genes, including those that perform initial oxidation and dehydrogenation reactions and those that further degrade the resulting substrates into small molecules; and metabolism genes that complete the intracellular transformation and utilization of estrogen metabolites through biological processes such as amino acid metabolism, lipid metabolism, carbohydrate metabolism, and the tricarboxylic acid cycle. In summary, the biodegradation of estrogens is coordinated by a metabolic network of estrogen-degrading enzymes, transporters, metabolic enzymes, and other coenzymes. In this study, the metabolic mechanisms by which Rhodococcus equi R-001 degrades various estrogens were analyzed for the first time. A new pollutant metabolism system is outlined, providing a starting point for the construction of engineered estrogen-degrading bacteria.

As a widespread pollutant, bisphenol A (BPA) has created a serious threat to ecosystem and human health. Therefore, expanding the available microbial resources used to screen highly efficient BPA-degrading bacteria with BPA as the sole carbon source is very important for the removal of this pollutant from the environment. In this study, the BPA degradation rate of Pseudomonas sp. P1 to 30 mg/L was 96.89% within 120 h. Whole genome sequencing showed that the genome of strain P1 was composed of a single circular chromosome with a full length of 6.17 Mb, which contained 5636 predicted coding genes. Comparative genomic analysis showed that strain P1 contained 210 functional genes related to BPA degradation. It was confirmed that BPA degradation genes ferredoxin (bisdA), P450 (bisdB), CotA and Lac in strain P1 were highly expressed under the induction of BPA. Combined with the identification of metabolites, the route of BPA degradation by Pseudomonas was proposed. A new metabolite, 4-vinylphenol, was detected for the first time in pathway Ⅰ. In pathway Ⅱ, BPA is directly oxidized to phenol and 4-isopropenyl phenol in the presence of laccase, which is rarely reported in the process of bacterial degradation of BPA. This study confirmed that strain P1 had good tolerance to various environmental factors at the gene level and enriched the degradation mechanism of BPA.

This study assessed the toxic effects of bisphenol A (BPA) on the microbial community and the function of activated sludge in sequencing batch reactors (SBRs). The toxicity of BPA was mitigated through dosing sludge with Rhodococcus Req-001. BPA reduced the biomass of sludge, and the proportion of viable bacteria decreased with the aggravation of BPA pollution. BPA affected the secretion of extracellular polymeric substances (EPSs), increased the ratio of polysaccharide to protein, and deteriorated the sedimentation performance of sludge. BPA decreased the abundances of functional bacteria involved in the degradation of organic matter and water purification, including Polaromonas, Dechloromonas, and Nitrospira, and the water purification capacity of the reactor decreased. Req-001 enhanced the BPA removal efficiency by 15%, and increased ammonia nitrogen and phosphorus removal by 8.8% and 22.7%, respectively. The functional recovery ability of the sludge system and the high removal ability of Req-001 make it a promising specie for use in BPA bioremediation. This study combined the effect of BPA on activated sludge and reactor performance with the microbial community, clarified the toxic mechanism of BPA on activated sludge, and therefore provides a theoretical basis and potential solutions to help WWTPs cope with the toxic effects of BPA.

Signaling molecules, particularly acyl-homoserine lactones (AHLs), can enhance microbial activity under low-temperature stress. However, the specific mechanisms underlying this effect remain unclear. This study identified a typical activated sludge functional bacterium that is sensitive to low temperatures and regulated by hexanoyl-L-homoserine lactone (C6-HSL), a representative of AHLs. It elucidates how C6-HSL modulates the bacterium's resistance to low-temperature stress. Experimental results indicated that C6-HSL significantly increased the levels of adenosine triphosphate (ATP), superoxide dismutase (SOD), peroxidase (POD) and glutathione peroxidase (GSH-Px) in strain LB-001 under low-temperature stress, while also decreasing the levels of reactive oxygen species (ROS). Additionally, C6-HSL markedly repaired the damage to cell membrane structure caused by low-temperature stress. At the genetic level, C6-HSL upregulated the expression of 20 key genes related to energy metabolism, antioxidation, and fatty acid synthesis. At the metabolic level, C6-HSL increased the levels of metabolites related to energy metabolism and antioxidation, boosted the content of unsaturated fatty acids, and reduced the content of saturated fatty acids. This study utilized C6-HSL and low-temperature induction in conjunction with 16S microbial diversity sequencing, genomics, transcriptomics, and metabolomics. These methods were employed to elucidate the molecular mechanisms by which exogenous C6-HSL regulates the resistance of activated sludge microbial communities to low-temperature stress. This research lays the foundation for the application of AHLs and cell communication in wastewater biological treatment, fostering deeper exploration and further innovation in related academic research.