Sun Lijing, Sheng Qi, Wang Shuyue, He Linyan, Sheng Xiafang
College of Life Sciences, Nanjing Agricultural University, Key Laboratory of Agricultural and Environmental Microbiology, Ministry of Agriculture, Nanjing 210095, China.
College of Life Sciences, Nanjing Agricultural University, Key Laboratory of Agricultural and Environmental Microbiology, Ministry of Agriculture, Nanjing 210095, China.
Microbiol Res. 2025 Nov;300:128277. doi: 10.1016/j.micres.2025.128277. Epub 2025 Jul 8.
Understanding the molecular mechanisms underlying bacteria-mediated cadmium (Cd) stabilization is crucial for enhancing Cd remediation in solution. Although the quorum-sensing SinI/SinR system (SIRS) contributes to Cd stabilization by Ensifer adhaerens, its molecular mechanisms remain poorly understood. In this study, we characterized the molecular mechanisms associated with the quorum-sensing SIRS-regulated Cd stabilization of strain NER9 in a Cd-containing solution. Transcriptomic analysis revealed that the expression levels of Cd stabilization-related genes associated with cell wall/cell membrane components (mprF, pA_gene1260, pA_gene1253, and pA_gene1263), exopolysaccharide production (melA, rfbB, and rfbA), and membrane proteins (omp31, pA_gene1257, and pC_gene0059) were downregulated in the NER9ΔsinI/R mutant compared with those in NER9. Metabolomic analysis further revealed that the Cd-immobilizing related intracellular metabolites involved in cell wall/cell membrane components were downregulated in the NER9ΔsinI/R mutant compared with those in NER9. Real-time reverse transcription-quantitative PCR analysis confirmed that the expression levels of Cd immobilization-related genes mprF, rfbB, rfbA, omp31, pA_gene1260, pA_gene1253, pA_gene1263, pA_gene1257 and pC_gene0059 were downregulated in the mutant NER9ΔsinI/R compared with those in NER9 under Cd-free and Cd-containing conditions. Notably, in the presence of the gene deletion mutants NER9ΔrfbA/B, NER9ΔpA_1263, and NER9ΔpA_1260, solution Cd concentrations increased significantly by 37 %-65 %, while cell surface-adsorbed Cd levels decreased by 57 %-61 % compared to those in the presence of NER9 after 16 h of incubation. Our findings suggest that the SIRS of NER9 contributes to Cd stabilization by upregulating the expression of genes and intracellular metabolites associated with cell surface and exopolysaccharide-mediated Cd adsorption in Cd-contaminated solutions.
了解细菌介导的镉（Cd）稳定化的分子机制对于增强溶液中的镉修复至关重要。虽然群体感应SinI/SinR系统（SIRS）有助于粘附剑菌对镉的稳定化，但其分子机制仍知之甚少。在本研究中，我们表征了在含镉溶液中与群体感应SIRS调节的NER9菌株镉稳定化相关的分子机制。转录组分析表明，与细胞壁/细胞膜成分（mprF、pA_gene1260、pA_gene1253和pA_gene1263）、胞外多糖产生（melA、rfbB和rfbA）以及膜蛋白（omp31、pA_gene1257和pC_gene0059）相关的镉稳定化相关基因的表达水平在NER9ΔsinI/R突变体中比在NER9中下调。代谢组分析进一步表明，与NER9相比，NER9ΔsinI/R突变体中参与细胞壁/细胞膜成分的镉固定相关细胞内代谢物下调。实时逆转录定量PCR分析证实，在无镉和含镉条件下，与NER9相比，突变体NER9ΔsinI/R中镉固定相关基因mprF、rfbB、rfbA、omp31、pA_gene1260、pA_gene1253、pA_gene1263、pA_gene1257和pC_gene0059的表达水平下调。值得注意的是，在基因缺失突变体NER9ΔrfbA/B、NER9ΔpA_1263和NER9ΔpA_1260存在的情况下，孵育16小时后，溶液中的镉浓度显著增加了37%-65%，而细胞表面吸附的镉水平与存在NER9时相比降低了57%-61%。我们的研究结果表明，NER9的SIRS通过上调与细胞表面和胞外多糖介导的镉吸附相关的基因和细胞内代谢物的表达，有助于镉的稳定化。
