The genome sequence of <i>Bifidobacterium longum</i> subsp. <i>infantis</i> reveals adaptations for milk utilization within the infant microbiome

TLDR

Following birth, the breast‑fed infant gut is rapidly colonized by bifidobacteria. Several chromosomal loci, including a 43 kbp cluster of catabolic genes, extracellular solute‑binding proteins, and permeases, are predicted to be active on milk oligosaccharides, indicating adaptation to the infant host. The genome of *Bifidobacterium longum* subsp.

Abstract

Following birth, the breast-fed infant gastrointestinal tract is rapidly colonized by a microbial consortium often dominated by bifidobacteria. Accordingly, the complete genome sequence of Bifidobacterium longum subsp. infantis ATCC15697 reflects a competitive nutrient-utilization strategy targeting milk-borne molecules which lack a nutritive value to the neonate. Several chromosomal loci reflect potential adaptation to the infant host including a 43 kbp cluster encoding catabolic genes, extracellular solute binding proteins and permeases predicted to be active on milk oligosaccharides. An examination of in vivo metabolism has detected the hallmarks of milk oligosaccharide utilization via the central fermentative pathway using metabolomic and proteomic approaches. Finally, conservation of gene clusters in multiple isolates corroborates the genomic mechanism underlying milk utilization for this infant-associated phylotype.