ArticleNature communications2026
Heterogeneity in the response to the metabolic environment drives fosfomycin heteroresistance.
Jacob E Choby, David A Hufnagel, Muqing Ma, Tugba Ozturk, Victor I Band, Minsu Kim, David S Weiss
Abstract read
In one paragraphArticle in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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.
2 · The registryThe 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.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
7 authors.
David A Hufnagel *Emory Antibiotic Resistance Center, Atlanta, GA, USA.
Tugba OzturkEmory Antibiotic Resistance Center, Atlanta, GA, USA.
David S WeissEmory Antibiotic Resistance Center, Atlanta, GA, USA. david.weiss@emory.edu.
Funding
Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0MSingle Cell Analysis Core (Core C)U19AI158080 · NIAID · EMORY UNIVERSITY · PI LEVIN, BRUCE RICHARD, WEISS, DAVID S · 2021 to 2025
$10.9MBETA-LACTAMASE MUTATIONS IN ANTIBIOTIC RESISTANCER01AI032956 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI Timothy Palzkill · 1992 to 2026
$6.5MBeta Lactamase Mutations in Antibiotic ResistanceR37AI032956 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI PALZKILL, TIMOTHY · 2001 to 2010
$3.3MHeteroresistance Interdisciplinary Research Unit: Quantitative Analysis and Single-Cell Microscopy Core (Core C)P01AI197193 · NIAID · EMORY UNIVERSITY · PI DAVID S WEISS · 2026 to 2026
$2.9MResearch Training in Translational Gastroenterology and HepatologyT32DK108735 · NIDDK · EMORY UNIVERSITY · PI SUBRA KUGATHASAN · 2016 to 2026
$2.6MMechanisms of phenotypic antibiotic resistance in Gram-negative bacteriaR01AI141883 · NIAID · EMORY UNIVERSITY · PI WEISS, DAVID S · 2018 to 2022
$2.2MBeta Lactamase Mutations in Antibiotic ResistanceR56AI032956 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI PALZKILL, TIMOTHY · 2016 to 2016
$394kCystic Fibrosis Foundation (CF Foundation) CHOBY19F0NIAID NIH HHS P01 AI197193NIAID NIH HHS R01 AI032956NIAID NIH HHS R01 AI141883NIAID NIH HHS R37 AI032956NIAID NIH HHS R56 AI032956NIAID NIH HHS U19 AI158080NIDDK NIH HHS T32 DK108735NIH HHS P51 OD011132U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI141883U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI158080U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI197193U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI32956U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) T32 DK108735U.S. Department of Health & Human Services | NIH | NIH Office of the Director (OD) P51 OD011132
6 · The paper itselfAbstract
Heteroresistance is a form of antibiotic resistance in which a phenotypically unstable subpopulation of resistant cells coexists with a majority susceptible population. Many mechanisms of heteroresistance are unclear and the impact of the extracellular environment on this phenomenon is unknown. Studying fosfomycin heteroresistance in Enterobacter cloacae complex, we observed that glucose availability greatly increased the frequency of the resistant subpopulation. Glucose downregulated the glycerol and fosfomycin importer GlpT via catabolite repression. Heteroresistance was generated by heterogeneity in single-cell expression of GlpT, in addition to expression of fosA, which acted as a resistance enhancer. Due to the impact of environmental glucose on glpT expression, we observed that the resistant subpopulation was more frequent during infection in murine models of hyperglycemia/diabetes. Thus, we reveal a paradigm where heterogeneity in response to the environment tunes resistant subpopulation frequency, which suggests that the metabolic context of infection in specific disease states may be important to consider in treatment decisions.
Indexed as
Anti-Bacterial AgentsDrug Resistance, BacterialEnterobacter cloacaeFosfomycinAnimalsBacterial ProteinsGene Expression Regulation, BacterialGlucoseGlycerolMiceMicrobial Sensitivity TestsAnti-Bacterial AgentsBacterial ProteinsFosfomycinGlucoseGlycerol
Identifiers
PMID42830333
PMCPMC13635211
What OpenQuestion holds
Textmetadata
Read underepoch 390