The proliferation of cyanobacterial blooms poses a significant threat to aquatic ecosystems and drinking water safety. Traditional control strategies mainly focus on environmental factors and overlook microbial communication networks. This study systematically elucidated the quorum sensing (QS) system in Microcystis aeruginosa and identified a previously unknown QS signaling molecule N-carboxy-C₁₀-homoserine lactone (N-carboxy-C₁₀-HSL), and its homologous synthase and receptor in the genome for MaeI/MaeR through ultra-high resolution mass spectrometry and genomics methods. These findings provide precise targets for disrupting the QS regulation of M. aeruginosa. As a biocompatible quorum quencher, indole achieved a 95.3 % inhibition rate within 14 days at 0.55 mM. Mechanistically, sub-inhibitory indole (0.07 mM) down-regulates the transcripts of maeI and maeR by 31 % and 38 %, suppressing QS regulation, while higher doses (EC₅₀) induced membrane perturbation and reactive oxygen species (ROS)‑mediated oxidative stress, as evidenced by an 88.6 % decrease in PSII quantum efficiency and a 14.6‑fold increase in malondialdehyde (MDA) levels. Molecular docking confirmed its unique competitive inhibition of AHL MaeR binding through hydrogen bonding (-4.8 kcal/mol) with ASP101 (A). Unlike traditional algaecides, this method significantly reduces the production of microcystin-LR and ecological risks by targeted downregulation of maeI/maeR. These findings indicate that quorum quenching is a promising sustainable algal bloom mitigation strategy that can protect aquatic ecosystems by simultaneously controlling algal proliferation and toxin production.

中文翻译：

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吲哚竞争性抑制群体感应并触发氧化应激以抑制微囊藻华

蓝藻水华的扩散对水生生态系统和饮用水安全构成重大威胁。传统的防治策略主要关注环境因素，而忽视了微生物通讯网络。本研究系统阐明了铜绿微囊藻中的群体感应 （QS） 系统，并通过超高分辨率质谱和基因组学方法鉴定了以前未知的 QS 信号分子 N-羧基-C ₁₀ -高丝氨酸内酯 （N-carboxy-C ₁₀ -HSL） 及其在基因组中对 MaeI/MaeR 的同源合酶和受体。这些发现为破坏铜绿分枝杆菌的 QS 调节提供了精确的靶点。作为生物相容性群体淬灭剂，吲哚在 0.55 mM 时在 14 天内达到 95.3% 的抑制率。从机制上讲，亚抑制性吲哚 （0.07 mM） 将 maeI 和 maeR 的转录物下调 31% 和 38%，抑制 QS 调节，而较高剂量 （EC ₅₀ ） 诱导膜扰动和活性氧 （ROS） 介导的氧化应激，PSII 量子效率降低 88.6% 和丙二醛 （MDA） 水平增加 14.6 倍。分子对接证实了其通过与 ASP101 （A） 的氢键 （-4.8 kcal/mol） 对 AHL MaeR 结合的独特竞争性抑制。与传统的灭藻剂不同，这种方法通过靶向下调 maeI/maeR 显着减少了微囊藻毒素-LR 的产生和生态风险。这些发现表明，群体猝灭是一种很有前途的可持续藻华缓解策略，它可以通过同时控制藻类增殖和毒素产生来保护水生生态系统。