The arginine repressor ArgR controls virulence factors of adherent-invasive Escherichia coli strains
- 1Microbiology of Intestinal Diseases, Biology Department, Universitat de Girona, Girona, Spain.
Abstract
Introduction: Adherent-invasive Escherichia coli (AIEC) has been related to the physiopathology of Crohn’s disease, yet its pathogenic mechanisms are not completely understood. Arginine biosynthesis genes are upregulated in AIEC strains compared to non-AIEC strains present in the supernatant of infected intestinal epithelial cells, suggesting that arginine biosynthesis may be involved in AIEC pathogenicity.
Methods: To test this hypothesis, the argR gene, encoding the transcriptional repressor ArgR, was deleted in the AIEC strains AIEC16 and LF82, and in E. coli Nissle 1917 and K-12 C600, leading to increased expression of arginine biosynthesis genes. Phenotypic assays and transcriptomic analyses were conducted to assess differences between mutants (ΔargR) and wild-type (WT) strains.
Results: The absence of ArgR led to a more invasive and motile AIEC LF82 strain. No differences in invasion were found for AIEC16 and the mutation led to reduced motility and biofilm formation in this strain. Transcriptomic analysis was in line with the phenotypic observations and further revealed that ArgR regulates the expression of multiple virulence-associated genes. Acid resistance genes (gad operon) were upregulated in ΔargR strains, indicating a repressive role of ArgR. Conversely, genes involved in adhesion, lipopolysaccharide biosynthesis, and iron uptake were downregulated in mutant strains, suggesting that ArgR functions as an activator for these pathways.
Discussion: These findings highlight ArgR as a potential modulator of multiple virulence traits, influencing the invasive and adaptive capabilities of AIEC.
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BibTeX
@article{bonetrossinyol2026arginine,
title = {{The arginine repressor ArgR controls virulence factors of adherent-invasive Escherichia coli strains}},
author = {Queralt Bonet-Rossinyol and Margarita Martinez-Medina and Llorenç Fernández-Coll},
journal = {Frontiers in Cellular and Infection Microbiology},
year = {2026},
month = oct,
doi = {10.3389/fcimb.2026.1941024},
url = {https://doi.org/10.3389/fcimb.2026.1941024},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The arginine repressor ArgR controls virulence factors of adherent-invasive Escherichia coli strains
AU - Queralt Bonet-Rossinyol
AU - Margarita Martinez-Medina
AU - Llorenç Fernández-Coll
PY - 2026
DA - 2026/10/12
JO - Frontiers in Cellular and Infection Microbiology
DO - 10.3389/fcimb.2026.1941024
UR - https://doi.org/10.3389/fcimb.2026.1941024
AB - Introduction: Adherent-invasive Escherichia coli (AIEC) has been related to the physiopathology of Crohn’s disease, yet its pathogenic mechanisms are not completely understood. Arginine biosynthesis genes are upregulated in AIEC strains compared to non-AIEC strains present in the supernatant of infected intestinal epithelial cells, suggesting that arginine biosynthesis may be involved in AIEC pathogenicity. Methods: To test this hypothesis, the argR gene, encoding the transcriptional repressor ArgR, was deleted in the AIEC strains AIEC16 and LF82, and in E. coli Nissle 1917 and K-12 C600, leading to increased expression of arginine biosynthesis genes. Phenotypic assays and transcriptomic analyses were conducted to assess differences between mutants (ΔargR) and wild-type (WT) strains. Results: The absence of ArgR led to a more invasive and motile AIEC LF82 strain. No differences in invasion were found for AIEC16 and the mutation led to reduced motility and biofilm formation in this strain. Transcriptomic analysis was in line with the phenotypic observations and further revealed that ArgR regulates the expression of multiple virulence-associated genes. Acid resistance genes (gad operon) were upregulated in ΔargR strains, indicating a repressive role of ArgR. Conversely, genes involved in adhesion, lipopolysaccharide biosynthesis, and iron uptake were downregulated in mutant strains, suggesting that ArgR functions as an activator for these pathways. Discussion: These findings highlight ArgR as a potential modulator of multiple virulence traits, influencing the invasive and adaptive capabilities of AIEC.
SN - 2235-2988
ER -