Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, China.
NPJ Biofilms Microbiomes. 2020 May 20;6(1):22. doi: 10.1038/s41522-020-0132-3.
Aeromonas hydrophila is the causative agent of motile Aeromonad septicemia in fish. Previous studies have shown that the myo-inositol metabolism is essential for the virulence of this bacterium. IolR is a transcription inhibitor that negatively regulates myo-inositol metabolic activity. While in the process of studying the inositol catabolism in A. hydrophila Chinese epidemic strain NJ-35, we incidentally found that ΔiolR mutant exhibited obvious autoaggregation and increased biofilm formation compared to the wild type. The role of surface proteins in A. hydrophila autoaggregation was confirmed by different degradation treatments. Furthermore, calcium promotes the formation of aggregates, which disappear in the presence of the calcium chelator EGTA. Transcriptome analysis, followed by targeted gene deletion, demonstrated that biofilm formation and autoaggregation caused by the inactivation of iolR was due to the increased transcription of a RTX-family adhesion gene, rmpA. Further, IolR was determined to directly regulate the transcription of rmpA. These results indicated that iolR is negatively involved in autoaggregation and biofilm formation in A. hydrophila, and this involvement was associated with its inhibition on the expression of rmpA.
气单胞菌是鱼类游动气单胞菌败血症的病原体。先前的研究表明，肌醇代谢对该细菌的毒力至关重要。IolR 是一种转录抑制剂，可负调控肌醇代谢活性。在研究中国流行株 NJ-35 的肌醇分解代谢过程中，我们偶然发现与野生型相比，ΔiolR 突变体表现出明显的自聚集和生物膜形成增加。通过不同的降解处理证实了表面蛋白在气单胞菌自聚集中的作用。此外，钙促进聚集物的形成，而在钙螯合剂 EGTA 存在下聚集物消失。转录组分析，随后进行靶向基因缺失，表明 iolR 的失活导致生物膜形成和自聚集是由于 RTX 家族黏附基因 rmpA 的转录增加。此外，确定 IolR 直接调节 rmpA 的转录。这些结果表明，iolR 负调控气单胞菌的自聚集和生物膜形成，这种调控与它对 rmpA 表达的抑制有关。
