Tang Hao, Zhan Ziyang, Liu Xiucheng, Huang Xinxiang
Department of Clinical Laboratory, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Department of Biochemistry & Molecular Biology, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Future Microbiol. 2025 Mar;20(4):295-303. doi: 10.1080/17460913.2025.2460338. Epub 2025 Jan 30.
This study aims to explore the role of propionylation at the K32 residue of the global regulator Fis in serovar Typhi (. Typhi) and its influence on the pathogenicity of the bacteria.
MATERIALS & METHODS: Bacterial strains were cultured in media with sodium propionate supplementation. The propionylation status of Fis was determined through Western blot and mass spectrometry analyses. The DNA-binding capability of Fis was assessed using EMSA. The invasion and survival capacities of . Typhi were examined using T84 cells and THP-1 macrophages.
Propionylation at the K32 site of Fis was found to down-regulate its DNA-binding ability, leading to a reduction in the invasion and survival of . Typhi within host cells. The K32Q mutant exhibited significantly decreased invasion and survival capabilities compared to the wild-type and K32R mutant strains.
Propionylation of Fis at the K32 residue impacts the pathogenicity of . Typhi, shedding light on the role of post-translational modifications in bacterial infections.
本研究旨在探讨全局调节因子Fis的K32残基丙酰化在伤寒杆菌(伤寒沙门氏菌)中的作用及其对细菌致病性的影响。
将细菌菌株在添加丙酸钠的培养基中培养。通过蛋白质免疫印迹和质谱分析确定Fis的丙酰化状态。使用电泳迁移率变动分析(EMSA)评估Fis的DNA结合能力。使用T84细胞和THP-1巨噬细胞检测伤寒沙门氏菌的侵袭和存活能力。
发现Fis的K32位点丙酰化会下调其DNA结合能力,导致伤寒沙门氏菌在宿主细胞内的侵袭和存活减少。与野生型和K32R突变株相比,K32Q突变体的侵袭和存活能力显著降低。
Fis在K32残基处的丙酰化影响伤寒沙门氏菌的致病性,揭示了翻译后修饰在细菌感染中的作用。