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β‐Glucan is a major growth substrate for human gut bacteria related to Coprococcus eutactus

Anna M. Alessi; Victoria Gray; Freda M. Farquharson; Adriana Flores‐López; Sophie Shaw; David Stead; Udo Wegmann; Claire Shearman; Mike Gasson; Elaina S. R. Collie‐Duguid; Harry J. Flint; Petra Louis
Environmental Microbiology · Vol. 22, Issue 6 · pp. 2150-2164 · 2020

Abstract

Summary A clone encoding carboxymethyl cellulase activity was isolated during functional screening of a human gut metagenomic library using Lactococcus lactis MG1363 as heterologous host. The insert carried a glycoside hydrolase family 9 (GH9) catalytic domain with sequence similarity to a gene from Coprococcus eutactus ART55/1. Genome surveys indicated a limited distribution of GH9 domains among dominant human colonic anaerobes. Genomes of C. eutactus ‐related strains harboured two GH9‐encoding and four GH5‐encoding genes, but the strains did not appear to degrade cellulose. Instead, they grew well on β‐glucans and one of the strains also grew on galactomannan, galactan, glucomannan and starch. Coprococcus comes and Coprococcus catus strains did not harbour GH9 genes and were not able to grow on β‐glucans. Gene expression and proteomic analysis of C. eutactus ART55/1 grown on cellobiose, β‐glucan and lichenan revealed similar changes in expression in comparison to glucose. On β‐glucan and lichenan only, one of the four GH5 genes was strongly upregulated. Growth on glucomannan led to a transcriptional response of many genes, in particular a strong upregulation of glycoside hydrolases involved in mannan degradation. Thus, β‐glucans are a major growth substrate for species related to C. eutactus , with glucomannan and galactans alternative substrates for some strains.

Bibliographic Information

JournalEnvironmental Microbiology
PublisherWiley
Publication Date2020-06-01
Publication Year2020
Volume22
Issue6
Pages2150-2164
Document TypeJournal Article
Print ISSN1462-2912
eISSN1462-2920
DOI10.1111/1462-2920.14977
SubjectMicrobial Ecology

Access Information

NARA Access Coverage1999-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/14622920
Publisher PageOpen Publisher Page
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