将细胞壁结合的多糖转换为乳酸菌中分泌的多糖
Saulius Kulakauskas1, Irina Sadovskaya2, Evgeny Vinogradov3
1Université Paris-Saclay, INRAE, AgroParisTech, Micalis Institute, Jouy-en-Josas, France.
Carbohydrate polymers
|March 14, 2026
概括
突变的乳酸菌因EpsD氨酸激酶的缺陷而过度产生细菌外聚糖 (EPS). 这种从细胞壁结合的多糖到分泌的EPS的转换与自酸化受损有关.
科学领域:
- 微生物学 微生物学
- 生物化学 生物化学
- 分子生物学分子生物学
背景情况:
- 细菌外聚糖 (EPS) 是有价值的碳水化合物聚合物,在食品和健康领域有应用.
- 乳酸细菌产生具有有益性质的EPS.
- 了解EPS生产机制对于利用其潜力至关重要.
研究的目的:
- 为了识别导致EPS过度产生的遗传突变,在乳酸菌中.
- 阐明了从细胞壁结合的多糖转换到分泌的EPS的分子机制.
- 描述过度产生的EPS的结构及其与细胞壁相关的多糖的关系.
主要方法:
- 使用沉积率选择方法分离具有高EPS产量的自发乳酸菌突变体.
- 基因分析以确定Wzy依赖多糖生物合成集群中的基因突变,特别是epsC和epsD.
- 详细描述 Lacticaseibacillus rhamnosus 突变的特征,包括分析 EpsD 氨酸激酶活性和确定 EPS 结构.
主要成果:
- 获得了生产过多EPS的自发突变,经常在epsD (编码氨酸激酶) 中表现出错误的突变或在epsC (编码其调节器) 中插入.
- 发现EpsD催化部位的特定D94L突变抑制了其自酸化.
- 过度生产的EPS由酸盐替代剂的酸盐重复单元组成,结构上与野生型菌株中发现的细胞壁结合的多糖体完全相同.
结论:
- EpsD氨酸激酶的自酸化缺陷与从细胞壁结合的多糖转换到EPS释放到环境中的转换有关.
- 在epsD或epsC的突变可以导致多糖局部化和生产的显著改变.
- 这项研究提供了关于Lacticaseibacillus rhamnosus中EPS生物合成和分泌的调节的见解.
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