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Chemotaxis and autoinducer-2 signalling mediate colonization and contribute to co-existence of Escherichia coli strains in the murine gut

Laganenka, Leanid; Lee, Jae-Woo; Malfertheiner, Lukas; Dieterich, Cora Lisbeth; Fuchs, Lea; Piel, Jörn; von Mering, Christian; Sourjik, Victor; Hardt, Wolf-Dietrich (2023). Chemotaxis and autoinducer-2 signalling mediate colonization and contribute to co-existence of Escherichia coli strains in the murine gut. Nature Microbiology, 8(2):204-217.

Abstract

Bacteria communicate and coordinate their behaviour at the intra- and interspecies levels by producing and sensing diverse extracellular small molecules called autoinducers. Autoinducer 2 (AI-2) is produced and detected by a variety of bacteria and thus plays an important role in interspecies communication and chemotaxis. Although AI-2 is a major autoinducer molecule present in the mammalian gut and can influence the composition of the murine gut microbiota, its role in bacteria-bacteria and bacteria-host interactions during gut colonization remains unclear. Combining competitive infections in C57BL/6 mice with microscopy and bioinformatic approaches, we show that chemotaxis (cheY) and AI-2 signalling (via lsrB) promote gut colonization by Escherichia coli, which is in turn connected to the ability of the bacteria to utilize fructoselysine (frl operon). We further show that the genomic diversity of E. coli strains with respect to AI-2 signalling allows ecological niche segregation and stable co-existence of different E. coli strains in the mammalian gut.

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:07 Faculty of Science > Institute of Molecular Life Sciences
Dewey Decimal Classification:570 Life sciences; biology
Scopus Subject Areas:Life Sciences > Microbiology
Life Sciences > Immunology
Life Sciences > Applied Microbiology and Biotechnology
Life Sciences > Genetics
Health Sciences > Microbiology (medical)
Life Sciences > Cell Biology
Language:English
Date:9 January 2023
Deposited On:15 Feb 2023 08:56
Last Modified:29 Oct 2024 02:37
Publisher:Nature Publishing Group
ISSN:2058-5276
OA Status:Closed
Publisher DOI:https://doi.org/10.1038/s41564-022-01286-7
PubMed ID:36624229

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