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Fucose Sensing Regulates Bacterial Intestinal Colonization
The mammalian gastrointestinal (GI) tract provides a complex and competitive environment for the microbiota(1). Successful colonization by pathogens depends on scavenging nutrients, sensing chemical signals, competing with the resident bacteria, and precisely regulating expression of virulence genes...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518558/ https://www.ncbi.nlm.nih.gov/pubmed/23160491 http://dx.doi.org/10.1038/nature11623 |
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author | Pacheco, Alline R. Curtis, Meredith M. Ritchie, Jennifer M. Munera, Diana Waldor, Matthew K. Moreira, Cristiano G. Sperandio, Vanessa |
author_facet | Pacheco, Alline R. Curtis, Meredith M. Ritchie, Jennifer M. Munera, Diana Waldor, Matthew K. Moreira, Cristiano G. Sperandio, Vanessa |
author_sort | Pacheco, Alline R. |
collection | PubMed |
description | The mammalian gastrointestinal (GI) tract provides a complex and competitive environment for the microbiota(1). Successful colonization by pathogens depends on scavenging nutrients, sensing chemical signals, competing with the resident bacteria, and precisely regulating expression of virulence genes(2). The GI pathogen enterohemorrhagic E.coli (EHEC) relies on inter-kingdom chemical sensing systems to regulate virulence gene expression(3–4). Here we show that these systems control the expression of a novel two-component signal transduction system, named FusKR, where FusK is the histidine sensor kinase (HK), and FusR the response regulator (RR). FusK senses fucose and controls expression of virulence and metabolic genes. This fucose-sensing system is required for robust EHEC colonization of the mammalian intestine. Fucose is highly abundant in the intestine(5). Bacteroides thetaiotaomicron (B.theta) produces multiple fucosidases that cleave fucose from host glycans, resulting in high fucose availability in the gut lumen(6). During growth in mucin, B.theta contributes to EHEC virulence by cleaving fucose from mucin, thereby activating the FusKR signaling cascade, modulating EHEC’s virulence gene expression. Our findings suggest that EHEC uses fucose, a host-derived signal made available by the microbiota, to modulate EHEC pathogenicity and metabolism. |
format | Online Article Text |
id | pubmed-3518558 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
record_format | MEDLINE/PubMed |
spelling | pubmed-35185582013-06-06 Fucose Sensing Regulates Bacterial Intestinal Colonization Pacheco, Alline R. Curtis, Meredith M. Ritchie, Jennifer M. Munera, Diana Waldor, Matthew K. Moreira, Cristiano G. Sperandio, Vanessa Nature Article The mammalian gastrointestinal (GI) tract provides a complex and competitive environment for the microbiota(1). Successful colonization by pathogens depends on scavenging nutrients, sensing chemical signals, competing with the resident bacteria, and precisely regulating expression of virulence genes(2). The GI pathogen enterohemorrhagic E.coli (EHEC) relies on inter-kingdom chemical sensing systems to regulate virulence gene expression(3–4). Here we show that these systems control the expression of a novel two-component signal transduction system, named FusKR, where FusK is the histidine sensor kinase (HK), and FusR the response regulator (RR). FusK senses fucose and controls expression of virulence and metabolic genes. This fucose-sensing system is required for robust EHEC colonization of the mammalian intestine. Fucose is highly abundant in the intestine(5). Bacteroides thetaiotaomicron (B.theta) produces multiple fucosidases that cleave fucose from host glycans, resulting in high fucose availability in the gut lumen(6). During growth in mucin, B.theta contributes to EHEC virulence by cleaving fucose from mucin, thereby activating the FusKR signaling cascade, modulating EHEC’s virulence gene expression. Our findings suggest that EHEC uses fucose, a host-derived signal made available by the microbiota, to modulate EHEC pathogenicity and metabolism. 2012-11-18 2012-12-06 /pmc/articles/PMC3518558/ /pubmed/23160491 http://dx.doi.org/10.1038/nature11623 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms |
spellingShingle | Article Pacheco, Alline R. Curtis, Meredith M. Ritchie, Jennifer M. Munera, Diana Waldor, Matthew K. Moreira, Cristiano G. Sperandio, Vanessa Fucose Sensing Regulates Bacterial Intestinal Colonization |
title | Fucose Sensing Regulates Bacterial Intestinal Colonization |
title_full | Fucose Sensing Regulates Bacterial Intestinal Colonization |
title_fullStr | Fucose Sensing Regulates Bacterial Intestinal Colonization |
title_full_unstemmed | Fucose Sensing Regulates Bacterial Intestinal Colonization |
title_short | Fucose Sensing Regulates Bacterial Intestinal Colonization |
title_sort | fucose sensing regulates bacterial intestinal colonization |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518558/ https://www.ncbi.nlm.nih.gov/pubmed/23160491 http://dx.doi.org/10.1038/nature11623 |
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