An efficient and reproducible method for transformation of genetically recalcitrant bifidobacteria

This study describes an efficient transformation system for the introduction of plasmid DNA into Bifidobacterium bifidum PRL2010 and Bifidobacterium asteroides PRL2011, for which to the best of our knowledge no transformation data have been reported previously. The method is based on electroporation of bifidobacterial cells, which were made competent by an optimized methodology based on varying media and growth conditions. Furthermore, the transformation protocol was applied in order to design a PRL2010-derivative, which carries antibiotic resistance against chloramphenicol and which was used to monitor PRL2010 colonization in a murine model

Functional genome analysis of Bifidobacterium breve UCC2003 reveals type IVb tight adherence (Tad) pili as an essential and conserved host-colonization factor

Development of the human gut microbiota commences at birth, with bifidobacteria being among the first colonizers of the sterile newborn gastrointestinal tract. To date, the genetic basis of Bifidobacterium colonization and persistence remains poorly understood. Transcriptome analysis of the Bifidobacterium breve UCC2003 2.42-Mb genome in a murine colonization model revealed differential expression of a type IVb tight adherence (Tad) pilus-encoding gene cluster designated "tad(2003)." Mutational analysis demonstrated that the tad(2003) gene cluster is essential for efficient in vivo murine gut colonization, and immunogold transmission electron microscopy confirmed the presence of Tad pili at the poles of B. breve UCC2003 cells. Conservation of the Tad pilus-encoding locus among other B. breve strains and among sequenced Bifidobacterium genomes supports the notion of a ubiquitous pili-mediated host colonization and persistence mechanism for bifidobacteri

Author Correction: Metabolism of the predominant human milk oligosaccharide fucosyllactose by an infant gut commensal

The original version of this Article contained an error in Affiliation 4..