期刊
SCIENCE ADVANCES
卷 5, 期 8, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.aaw7696
关键词
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资金
- JSPS-KAKENHI [18K14379, 15H04481, 17K19231, 17J08530]
- Institute for Fermentation, Osaka [K-25-04]
- Independent Research Fund Denmark, Natural Sciences (DFF, FNU) [4002-00297B]
- Carlsberg Foundation [2011-01-0598]
- Danish Ministry of Higher Education and Science through the Instrument Center DANSCATT [7055-00005B]
- Grants-in-Aid for Scientific Research [18K14379, 17K19231, 15H04481, 17J08530] Funding Source: KAKEN
The human gut microbiota established during infancy has persistent effects on health. In vitro studies have suggested that human milk oligosaccharides (HMOs) in breast milk promote the formation of a bifidobacteria-rich microbiota in infant guts; however, the underlying molecular mechanism remains elusive. Here, we characterized two functionally distinct but overlapping fucosyllactose transporters (FL transporter-1 and -2) from Bifidobacterium longum subspecies infantis. Fecal DNA and HMO consumption analyses, combined with deposited metagenome data mining, revealed that FL transporter-2 is primarily associated with the bifidobacteria-rich microbiota formation in breast-fed infant guts. Structural analyses of the solute-binding protein (SBP) of FL transporter-2 complexed with 2'-fucosyllactose and 3-fucosyllactose, together with phylogenetic analysis of SBP homologs of both FL transporters, highlight a unique adaptation strategy of Bifidobacterium to HMOs, in which the gain-of-function mutations enable FL transporter-2 to efficiently capture major fucosylated HMOs. Our results provide a molecular insight into HMO-mediated symbiosis and coevolution between bifidobacteria and humans.
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