Bisphenol A (BPA) poses multiple risks to human health, and it has become a critical environmental pollution issue. The advantage of bacterial degradation of BPA has become more prominent, and enhancement methods have become increasingly diverse. Using quorum sensing to regulate functional bacteria and genes to enhance the bacterial degradation efficiency of BPA serves as a highly promising new approach. This study investigated the effect of adding exogenous N-hexanoyl-L-homoserine lactone (C6-HSL) on the degradation of BPA by Pseudomonas asiatica P1 (strain P1) and analyzed the regulatory mechanism of the signaling molecules. The results showed that exogenous homoserine lactone signaling molecules (AHLs) could enhance the BPA degradation efficiency of strain P1, with 10 μM C6-HSL demonstrating the most significant enhancement, increasing the degradation rate by 12.4 % compared with the control group and producing products such as benzoic acid and succinic acid. In terms of the regulatory mechanism, C6-HSL preferentially induced a 5.18-fold upregulation in the expression of the AHL receptor-encoding gene LasR. Subsequently, LasR regulates the upregulation of hub genes such as bvgS and aruS , ultimately achieving an upregulation of BPA degradation genes through hierarchical regulation. This led to an enhancement in the initial degradation step of BPA and the activation of the benzoic acid degradation pathway. This study analyzed the potential of C6-HSL to enhance microbial BPA degradation and, for the first time, clarified the mechanism by which C6-HSL enhanced bacterial BPA degradation efficiency through hierarchical regulation.
Bisphenol A (BPA) is a globally concerning toxic pollutant, and microbial degradation is considered an effective method to treat BPA contamination. However, the inherent microbial toxicity of BPA is often overlooked, particularly the microbial mechanisms of resistance and detoxification against BPA. This study found that under the toxic stress of BPA, cbb3-type cytochrome c oxidase (cbb3-Cox) in the cells of Pseudomonas asiatica P1 ( P. asiatica P1) was the first to resist the toxicity. Genes such as ccoNOQPG showed significant upregulation with an average log 2 FC value of 3.56. Subsequently, genes that are related to metal ion binding, transport, and DNA repair were upregulated in the middle to later phase, which enhanced the metabolic functions of the strains and induced strain mutations to assist P. asiatica P1 in resisting the BPA toxicity. Meanwhile, three potential BPA degradation genes were identified, among which sdr P1 was crucial to the BPA degradation and detoxification. After genetic recombination, sdr P1 achieved a degradation rate of 92.52 % for BPA. Furthermore, through various methods such as alkyl interactions, sdr P1 exhibited oxidation and demethylation to form lower toxic intermediate products and complete the biological detoxification of BPA. This study provides a systematic analysis of the toxicity resistance, biodegradation, and detoxification processes in bacterial BPA removal, refines the mechanism of BPA biodegradation and contributes to a more comprehensive and systematic understanding of the overall process of microbial removal of toxic pollutants.
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