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Title

A single mutation in the gene responsible for the mucoid phenotype of Bifidobacterium animalis subsp. lactis confers surface and functional characteristics

AuthorsHidalgo-Cantabrana, Claudio CSIC ORCID CVN; Sánchez García, Borja CSIC ORCID; Martínez Álvarez, Noelia CSIC ORCID CVN; Ruas-Madiedo, Patricia CSIC ORCID ; Margolles Barros, Abelardo CSIC ORCID
Issue Date11-Sep-2015
PublisherAmerican Society for Microbiology
CitationApplied and Environmental Microbiology 81(23): 7960-7968 (2015)
AbstractExopolysaccharides (EPS) are extracellular carbohydrate polymers synthesized by a large variety of bacteria. Their physiological functions have been extensively studied, but many of their roles have not yet been elucidated. We have sequenced the genomes of two isogenic strains of Bifidobacterium animalis subsp. lactis that differ in their EPS-producing phenotype. The original strain displays a nonmucoid appearance, and the mutant derived thereof has acquired a mucoid phenotype. The sequence analysis of their genomes revealed a nonsynonymous mutation in the gene Balat_1410, putatively involved in the elongation of the EPS chain. By comparing a strain from which this gene had been deleted with strains containing the wild-type and mutated genes, we were able to show that each strain displays different cell surface characteristics. The mucoid EPS synthesized by the strain harboring the mutation in Balat_1410 provided higher resistance to gastrointestinal conditions and increased the capability for adhesion to human enterocytes. In addition, the cytokine profiles of human peripheral blood mononuclear cells and ex vivo colon tissues suggest that the mucoid strain could have higher anti-inflammatory activity. Our findings provide relevant data on the function of Balat_1410 and reveal that the mucoid phenotype is able to alter some of the most relevant functional properties of the cells.
Publisher version (URL)https://doi.org/10.1128/AEM.02095-15
URIhttp://hdl.handle.net/10261/142755
DOI10.1128/AEM.02095-15
Identifiersissn: 0099-2240
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