Riboflavin Salvage Supports Glycolysis in Borrelia burgdorferi Through Flavin-Dependent NAD

Anna M Schulz, Grace E Easterling, Aaditya Balasubramaniyan, Mollie W Jewett

Abstract read

In one paragraph

Article in Molecular microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

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1 · What the graph read from it

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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.

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Anna M SchulzDivision of Immunity and Pathogenesis, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.

Grace E EasterlingDivision of Immunity and Pathogenesis, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.

Aaditya BalasubramaniyanDivision of Immunity and Pathogenesis, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.

Mollie W JewettDivision of Immunity and Pathogenesis, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.ORCID 0000-0003-3130-3795

Funding

Determination of the genetic basis for B. burgdorferi mammalian infectivityR01AI099094 · NIAID · UNIVERSITY OF CENTRAL FLORIDA · PI Mollie W Jewett · 2013 to 2026

$4.0M

NIAID NIH HHS R01 AI099094

6 · The paper itself

Abstract

Borrelia burgdorferi (Bb), the etiological agent of Lyme disease, lacks the genes for de novo riboflavin biosynthesis and depends on host-derived riboflavin to generate flavin cofactors FMN and FAD. Riboflavin salvage by Bb has demonstrated importance to infection and metabolic homeostasis, though the critical roles of flavin cofactors to central metabolism are not well defined. Here, we demonstrate that riboflavin availability directly controls glycolytic flux through regulation of intracellular redox balance. Disruption of riboflavin uptake by deletion of gene bb0318 encoding the putative ATPase component of the riboflavin transporter resulted in impaired glycolysis as indicated by reduced intracellular pyruvate and a perturbed NADH/NAD

Indexed as

Borrelia burgdorferiGlycolysisNADRiboflavinBacterial ProteinsFlavin-Adenine DinucleotideFlavinsMultienzyme ComplexesNADH, NADPH OxidoreductasesOxidation-ReductionBacterial ProteinsFlavin-Adenine DinucleotideFlavinsMultienzyme ComplexesNADNADH, NADPH OxidoreductasesNADH oxidaseRiboflavinBorrelia burgdorfericentral metabolismLyme diseaseNAD+ regenerationriboflavin salvage

Identifiers

PMID42381233

DOI10.1111/mmi.70090

PMCPMC13432742

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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.