Fucose Sensing Regulates Bacterial Intestinal Colonization

DSpace/Manakin Repository

Fucose Sensing Regulates Bacterial Intestinal Colonization

Citable link to this page


Title: Fucose Sensing Regulates Bacterial Intestinal Colonization
Author: Pacheco, Alline R.; Curtis, Meredith M.; Ritchie, Jennifer M.; Munera, Diana; Waldor, Matthew K.; Moreira, Cristiano G.; Sperandio, Vanessa

Note: Order does not necessarily reflect citation order of authors.

Citation: Pacheco, Alline R., Meredith M. Curtis, Jennifer M. Ritchie, Diana Munera, Matthew K. Waldor, Cristiano G. Moreira, and Vanessa Sperandio. 2012. “Fucose Sensing Regulates Bacterial Intestinal Colonization.” Nature 492 (7427): 113-117. doi:10.1038/nature11623. http://dx.doi.org/10.1038/nature11623.
Full Text & Related Files:
Abstract: The mammalian gastrointestinal (GI) tract provides a complex and competitive environment for the microbiota1. Successful colonization by pathogens depends on scavenging nutrients, sensing chemical signals, competing with the resident bacteria, and precisely regulating expression of virulence genes2. The GI pathogen enterohemorrhagic E.coli (EHEC) relies on inter-kingdom chemical sensing systems to regulate virulence gene expression3–4. 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 intestine5. Bacteroides thetaiotaomicron (B.theta) produces multiple fucosidases that cleave fucose from host glycans, resulting in high fucose availability in the gut lumen6. 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.
Published Version: doi:10.1038/nature11623
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518558/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11708577
Downloads of this work:

Show full Dublin Core record

This item appears in the following Collection(s)


Search DASH

Advanced Search