ArticleNature2012
Fucose sensing regulates bacterial intestinal colonization.
Article in Nature, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 299 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
299 citing papers in PubMed, 1 synthesis or guideline pooled it, 494 citations in OpenAlex.
- Association of Fucosyltransferase 2 Gene Variant with Inflammatory Bowel Diseases: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2019Pooled it
- A human milk oligosaccharide alters the microbiome, circulating hormones, and metabolites in a randomized controlled trial of older adults.Cell reports. Medicine · 2025Trial
- Neonatal intensive care unit (NICU) exposures exert a sustained influence on the progression of gut microbiota and metabolome in the first year of life.Scientific reports · 2021Trial
- Review
- L-fucose-dependent biofilm formation byBiofilm · 2026Article
- Mucin Increases the Virulence of EnterotoxigenicBiology · 2026Article
- Intestinal Fucosylation: A Key Regulatory Hub in Homeostasis and Disease Pathogenesis.Biomolecules · 2026Review
- Metabolic strategies of Enterobacteriaceae gut colonization.Nature reviews. Microbiology · 2026Review
- Orphan Enzymes in the Mammalian L-Fucose Degradation Pathway.Biomolecules · 2026Review
- L-Fucose-Dependent Biofilm Formation bybioRxiv : the preprint server for biology · 2026Article
- EnterohemorrhagiciScience · 2026Article
- Catabolism of serine enantiomers represses enterohemorrhagicProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Engineered bacterial therapy suppresses Enterohemorrhagic Escherichia coli through metabolic competition and virulence silencing.Nature communications · 2026Article
- Pathogenesis and therapeutic strategies in the interaction between gut microbiota and enterohemorrhagic Escherichia coli infection.FEMS microbiology reviews · 2026Review
- Ecology of the gut microbiota and colonization resistance: mechanisms and therapeutic implications.FEMS microbiology ecology · 2025Review
- Article
- Article
- l-Fucose is a candidate monosaccharide neuromodulator and mitigates Alzheimer's synaptic deficits.Science advances · 2025Article
- Itaconate utilisation by the human pathogen Pseudomonas aeruginosa requires uptake via the IctPQM TRAP transporter.The Biochemical journal · 2025Article
- An l-fucose-responsive transcription factor cross-regulates the expression of a diverse array of carbohydrate-active enzymes in Trichoderma reesei.PLoS genetics · 2025Article
239 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The mammalian gastrointestinal tract provides a complex and competitive environment for the microbiota. Successful colonization by pathogens requires scavenging nutrients, sensing chemical signals, competing with the resident bacteria and precisely regulating the expression of virulence genes. The gastrointestinal pathogen enterohaemorrhagic Escherichia coli (EHEC) relies on inter-kingdom chemical sensing systems to regulate virulence gene expression. 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 and FusR the response regulator. 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. Bacteroides thetaiotaomicron produces multiple fucosidases that cleave fucose from host glycans, resulting in high fucose availability in the gut lumen. During growth in mucin, B. thetaiotaomicron contributes to EHEC virulence by cleaving fucose from mucin, thereby activating the FusKR signalling cascade, modulating the virulence gene expression of EHEC. Our findings suggest that EHEC uses fucose, a host-derived signal made available by the microbiota, to modulate EHEC pathogenicity and metabolism.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.