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GalE's Role in Lipopolysaccharide O-Antigen Synthesis and Environmental Stress Resistance in STEC O5

文献类型： 外文期刊

作者： Deng, Yining 1 ; Zhang, Yunke 3 ; Wu, Tong 4 ; Peng, Chen 1 ; Wu, Wenxue 1 ;

作者机构： 1.China Agr Univ, Coll Vet Med, Natl Key Lab Vet Publ Hlth, Anim Dis Diagnost Lab, Beijing, Peoples R China

2.Texas A&M Univ, Coll Vet Med & Biomed Sci, College Stn, TX USA

3.Chinese Acad Med Sci & Peking Union Med Coll, Inst Lab Anim Sci, Beijing, Peoples R China

4.Chinese Acad Agr Sci, Biotechnol Res Inst, Beijing, Peoples R China

关键词： bacterial pathogenicity; complement killing; galE gene; lipopolysaccharide O-antigen; Shiga toxigenic Escherichia coli

期刊名称：JOURNAL OF BASIC MICROBIOLOGY （ 影响因子：2.7； 五年影响因子：3.5 ）

ISSN： 0233-111X

年卷期： 2025 年

页码：

收录情况： SCI

摘要： Shiga toxigenic Escherichia coli (STEC) is known to cause severe diarrhea and other gastrointestinal disorders in animals and humans. The galE gene encodes the galE protein, which acts as an essential catalyst required to convert UDP-galactose into UDP-glucose, and vital for exopolysaccharide synthesis. In this study, a knockout mutant of the STEC galE gene (Delta galE) was constructed and the biological functions of galE were analyzed. Relative to the wild-type strain, O-antigen synthesis within the Delta galE mutant changed and displayed distinct profiles via SDS-PAGE coupled with silver staining and Western blot analysis. Furthermore, this mutant showed a reduction in swimming motility, diminished biofilm formation, and reduced replication within macrophages. In the complement-killing assay, the membrane attack complex (MAC) was deposited in greater amounts on the Delta galE-deficient strain relative to the wild-type strain, indicating a higher susceptibility of the Delta galE strain toward complement-dependent lysis. However, the mutant manifested a more pronounced tolerance to extreme environments despite exhibiting comparable replication in a growth medium. These results indicate that galE plays a significant roles in O-antigen biosynthesis and contributes to STEC pathogenicity.

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