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首页> 外文期刊>Applied Microbiology >An l-Fucose Operon in the Probiotic Lactobacillus rhamnosus GG Is Involved in Adaptation to Gastrointestinal Conditions
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An l-Fucose Operon in the Probiotic Lactobacillus rhamnosus GG Is Involved in Adaptation to Gastrointestinal Conditions

机译:益生菌鼠李糖杆菌GG中的l-岩藻糖操纵子参与胃肠道疾病的适应。

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l-Fucose is a sugar present in human secretions as part of human milk oligosaccharides, mucins, and other glycoconjugates in the intestinal epithelium. The genome of the probiotic Lactobacillus rhamnosus GG (LGG) carries a gene cluster encoding a putative l-fucose permease ( fucP ), l-fucose catabolic pathway ( fucI , fucK , fucU , and fucA ), and a transcriptional regulator ( fucR ). The metabolism of l-fucose in LGG results in 1,2-propanediol production, and their fucI and fucP mutants displayed a severe and mild growth defect on l-fucose, respectively. Transcriptional analysis revealed that the fuc genes are induced by l-fucose and subject to a strong carbon catabolite repression effect. This induction was triggered by FucR, which acted as a transcriptional activator necessary for growth on l-fucose. LGG utilized fucosyl-α1,3- N -acetylglucosamine and contrarily to other lactobacilli, the presence of fuc genes allowed this strain to use the l-fucose moiety. In fucI and fucR mutants, but not in fucP mutant, l-fucose was not metabolized and it was excreted to the medium during growth on fucosyl-α1,3- N -acetylglucosamine. The fuc genes were induced by this fucosyl-disaccharide in the wild type and the fucP mutant but not in a fucI mutant, showing that FucP does not participate in the regulation of fuc genes and that l-fucose metabolism is needed for FucR activation. The l-fucose operon characterized here constitutes a new example of the many factors found in LGG that allow this strain to adapt to the gastrointestinal conditions.
机译:1-岩藻糖是人分泌物中存在的一种糖,是人肠上皮中的人乳寡糖,粘蛋白和其他糖结合物的一部分。益生菌鼠李糖乳杆菌GG(LGG)的基因组携带一个基因簇,该基因簇编码一个假定的l-岩藻糖通透酶(fucP),l-岩藻糖分解代谢途径(fucI,fucK,fucU和fucA)和一个转录调节因子(fucR)。 LGG中L-岩藻糖的代谢导致1,2-丙二醇的产生,它们的fucI和fucP突变体分别在L-岩藻糖上显示出严重的和轻度的生长缺陷。转录分析表明,fuc基因是由l-岩藻糖诱导的,并具有很强的碳分解代谢物抑制作用。该诱导是由FucR触发的,FucR充当在I-岩藻糖上生长所必需的转录激活因子。 LGG利用岩藻糖基-α1,3-N-乙酰基葡糖胺,与其他乳杆菌相反,fuc基因的存在使该菌株可以使用1-岩藻糖部分。在fucI和fucR突变体中,但在fucP突变体中没有,l-岩藻糖不被代谢,在岩藻糖基-α1,3-N-乙酰基葡糖胺上生长的过程中被分泌到培养基中。在野生型和fucP突变体中,这种岩藻糖基二糖诱导了fuc基因,但在fucI突变体中却没有,这表明FucP不参与fuc基因的调控,并且FucR激活需要l-岩藻糖代谢。此处表征的l-岩藻糖操纵子构成了LGG中发现的许多因素的新实例,这些因素使该菌株能够适应胃肠道疾病。

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