An l -Fucose Operon in the Probiotic Lactobacillus rhamnosus GG Is Involved in Adaptation to Gastrointestinal Conditions

• Published in: Applied and environmental microbiology Vol. 81; no. 11; pp. 3880 - 3888
• Main Authors: Becerra, Jimmy E., Yebra, María J., Monedero, Vicente
• Format: Journal Article
• Language: English
• Published: United States American Society for Microbiology 01.06.2015
• Subjects: Adaptation, Physiological; Culture Media - chemistry; Fucose - biosynthesis; Gastrointestinal Tract - microbiology; Gene Deletion; Gene Expression Profiling; Gene Expression Regulation, Bacterial; Genes; Genetics and Molecular Biology; Genomes; Humans; Lactobacillus rhamnosus - genetics; Lactobacillus rhamnosus - growth & development; Lactobacillus rhamnosus - physiology; Metabolic Networks and Pathways; Metabolism; Mucins; Mutants; Operon; Probiotics; Propylene Glycol - metabolism
• ISSN: 0099-2240; 1098-5336
• DOI: 10.1128/AEM.00260-15

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.