Peer-Reviewed Journal Details
Mandatory Fields
Turroni, F,Bottacini, F,Foroni, E,Mulder, I,Kim, JH,Zomer, A,Sanchez, B,Bidossi, A,Ferrarini, A,Giubellini, V,Delledonne, M,Henrissat, B,Coutinho, P,Oggioni, M,Fitzgerald, GF,Mills, D,Margolles, A,Kelly, D,van Sinderen, D,Ventura, M
2010
November
Proceedings of The National Academy of Sciences of The United States of America
Genome analysis of Bifidobacterium bifidum PRL2010 reveals metabolic pathways for host-derived glycan foraging
Validated
WOS: 230 ()
Optional Fields
coevolution genomics host-glycans metabolism human gut intestinal bacteria mucin ALPHA-N-ACETYLGALACTOSAMINIDASE HUMAN-MILK OLIGOSACCHARIDES GLYCOSIDE HYDROLASE FAMILY HUMAN INTESTINAL-TRACT HUMAN DISTAL GUT AKKERMANSIA-MUCINIPHILA MUCIN GLYCOPROTEINS MOLECULAR-CLONING LONGUM BACTERIAL
107
19514
19519
The human intestine is densely populated by a microbial consortium whose metabolic activities are influenced by, among others, bifidobacteria. However, the genetic basis of adaptation of bifidobacteria to the human gut is poorly understood. Analysis of the 2,214,650-bp genome of Bifidobacterium bifidum PRL2010, a strain isolated from infant stool, revealed a nutrient-acquisition strategy that targets host-derived glycans, such as those present in mucin. Proteome and transcriptome profiling revealed a set of chromosomal loci responsible for mucin metabolism that appear to be under common transcriptional control and with predicted functions that allow degradation of various O-linked glycans in mucin. Conservation of the latter gene clusters in various B. bifidum strains supports the notion that host-derived glycan catabolism is an important colonization factor for B. bifidum with concomitant impact on intestinal microbiota ecology.
10.1073/pnas.1011100107
Grant Details