# L-Arabinose Alters the E. coli Transcriptome to Favor Biofilm Growth and Enhances Survival During Fluoroquinolone Stress

**Authors:** Katherine M. Austin, Jenna K. Frizzell, Audrey A. Neighmond, Isabella J. Moppel, Lisa M. Ryno

PMC · DOI: 10.3390/microorganisms13071665 · 2025-07-15

## TL;DR

L-arabinose boosts biofilm growth in E. coli and reduces antibiotic effectiveness, especially at 37°C, by altering gene expression.

## Contribution

This study reveals a new role for L-arabinose in modulating biofilm and antibiotic resistance gene expression in E. coli.

## Key findings

- L-arabinose enhances biofilm growth at 37°C while reducing planktonic growth.
- L-arabinose decreases the efficacy of levofloxacin at sub-MIC concentrations.
- Transcriptomic analysis shows L-arabinose modulates antibiotic resistance and biofilm-related genes like fimA and csgA.

## Abstract

Environmental conditions, including nutrient composition and temperature, influence biofilm formation and antibiotic resistance in Escherichia coli. Understanding how specific metabolites modulate these processes is critical for improving antimicrobial strategies. Here, we investigated the growth and composition of Escherichia coli in both planktonic and biofilm states in the presence of L-arabinose, with and without exposure to the fluoroquinolone antibiotic levofloxacin, at two temperatures: 28 and 37 °C. At both temperatures, L-arabinose increased the growth rate of planktonic E. coli but resulted in reduced total growth; concurrently, it enhanced biofilm growth at 37 °C. L-arabinose reduced the efficacy of levofloxacin and promoted growth in sub-minimum inhibitory concentrations (25 ng/mL). Transcriptomic analyses provided insight into the molecular basis of arabinose-mediated reduced susceptibility of E. coli to levofloxacin. We found that L-arabinose had a temperature- and state-dependent impact on the transcriptome. Using gene ontology overrepresentation analyses, we found that L-arabinose modulated the expression of many critical antibiotic resistance genes, including efflux pumps (ydeA, mdtH, mdtM), transporters (proVWX), and biofilm-related genes for external structures like pili (fimA) and curli (csgA, csgB). This study demonstrates a previously uncharacterized role for L-arabinose in modulating antibiotic resistance and biofilm-associated gene expression in E. coli and provides a foundation for additional exploration of sugar-mediated antibiotic sensitivity in bacterial biofilms.

## Linked entities

- **Genes:** ydeA (arabinose efflux transporter) [NCBI Gene 917335], mdtH (multidrug resistance protein MdtH) [NCBI Gene 912474], mdtM (multidrug efflux system protein) [NCBI Gene 913623], fimA (major type 1 subunit fimbrin) [NCBI Gene 913688], csgA (curlin major subunit CsgA) [NCBI Gene 913991], csgB (curlin nucleator protein) [NCBI Gene 912479]
- **Chemicals:** L-arabinose (PubChem CID 439195), levofloxacin (PubChem CID 149096)
- **Species:** Escherichia coli (taxon 562)

## Full-text entities

- **Genes:** ydeA [NCBI Gene 2716519]
- **Diseases:** curli (MESH:C538074)
- **Chemicals:** L-arabinose (MESH:D001089), levofloxacin (MESH:D064704), Fluoroquinolone (MESH:D024841), sugar (MESH:D000073893)
- **Species:** Escherichia coli (E. coli, species) [taxon 562]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12299780/full.md

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Source: https://tomesphere.com/paper/PMC12299780