Data_Sheet_1_SdiA Enhanced the Drug Resistance of Cronobacter sakazakii and Suppressed Its Motility, Adhesion and Biofilm Formation.ZIP

Cronobacter sakazakii is a common foodborne pathogen, and the mortality rate of its infection is as high as 40–80%. SdiA acts as a quorum sensing regulator in many foodborne pathogens, but its role in C. sakazakii remains unclear. Here, we further determined the effect of the sdiA gene in C. sakazakii pathogenicity. The SdiA gene in C. sakazakii was knocked out by gene editing technology, and the biological characteristics of the ΔsdiA mutant of C. sakazakii were studied, followed by transcriptome analysis to elucidate its effects. The results suggested that SdiA gene enhanced the drug resistance of C. sakazakii but diminished its motility, adhesion and biofilm formation ability and had no effect on its growth. Transcriptome analysis showed that the ΔsdiA upregulated the expression levels of D-galactose operon genes (including dgoR, dgoK, dgoA, dgoD and dgoT) and flagella-related genes (FliA and FliC) in C. sakazakii and downregulated the expression levels of related genes in the type VI secretion system (VasK gene was downregulated by 1.53-fold) and ABC transport system (downregulated by 1.5-fold), indicating that SdiA gene was related to the physiological metabolism of C. sakazakii. The results were useful for clarifying the pathogenic mechanism of C. sakazakii and provide a theoretical basis for controlling bacterial infection.

克朗氏克朗菌 sakazakii 为一种常见食源性病原体，其感染死亡率高达40%-80%。SdiA 在众多食源性病原体中充当群体感应调节因子，但其在克朗氏克朗菌中的作用尚不明确。本研究进一步探究了 sdiA 基因对克朗氏克朗菌致病性的影响。通过基因编辑技术敲除克朗氏克朗菌中的 SdiA 基因，并研究其ΔsdiA 突变体的生物学特性，随后进行转录组分析以阐明其作用。结果表明，SdiA 基因增强了克朗氏克朗菌的耐药性，但降低了其运动性、粘附性和生物膜形成能力，对其生长无显著影响。转录组分析显示，ΔsdiA 突变体上调了克朗氏克朗菌中 D-半乳糖操纵子基因（包括 dgoR、dgoK、dgoA、dgoD 和 dgoT）和鞭毛相关基因（FliA 和 FliC）的表达水平，同时下调了与VI型分泌系统（VasK 基因下调1.53倍）和ABC转运系统（下调1.5倍）相关的基因表达水平，表明 SdiA 基因与克朗氏克朗菌的生理代谢相关。研究结果有助于阐明克朗氏克朗菌的致病机制，并为控制细菌感染提供了理论依据。