Genome analysis of <i>Bifidobacterium bifidum</i> PRL2010 reveals metabolic pathways for host-derived glycan foraging

TLDR

The human gut microbiome is dominated by bifidobacteria, yet the genetic mechanisms that enable these bacteria to adapt to the intestinal environment remain poorly understood. Genome, proteome, and transcriptome analyses of Bifidobacterium bifidum PRL2010 uncovered conserved loci that facilitate degradation of mucin‑derived glycans, highlighting glycan catabolism as a key colonization strategy that influences gut microbiota ecology.

Abstract

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.