Replication data for The arginine repressor ArgR controls virulence factors of Adherent-Invasive Escherichia coli strains

This dataset contains RNA‑sequencing data generated to investigate the regulatory role of the arginine repressor ArgR in Escherichia coli, with a focus on Adherent‑Invasive E. coli (AIEC), a pathotype associated with Crohn’s disease. Transcriptomes were obtained from four E. coli backgrounds—AIEC16,...

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Detalles Bibliográficos
Autores: Martinez-Medina, Margarita, Bonet Rossinyol, Queralt, Fernández-Coll, Llorenç
Tipo de recurso: conjunto de datos
Fecha de publicación:2026
País:España
Institución:Consorci de Serveis Universitaris de Catalunya (CSUC)
Repositorio:CORA.Repositori de Dades de Recerca
OAI Identifier:oai:dnet:cora.rdr____::6cfb0e7404ac374f8209cce187ee0e84
Acceso en línea:https://doi.org/10.34810/DATA3287
Access Level:acceso abierto
Palabra clave:Medicine, Health and Life Sciences
Adherent Invasive Escherichia coli
Escherichia coli
Escheríchia coli
Arginine
Arginine biosynthesis
Arginina -- Síntesi
Arginina -- Síntesis
Virulence regulation
Crohn's disease
Enteritis regional
Crohn, Malaltia de
Descripción
Sumario:This dataset contains RNA‑sequencing data generated to investigate the regulatory role of the arginine repressor ArgR in Escherichia coli, with a focus on Adherent‑Invasive E. coli (AIEC), a pathotype associated with Crohn’s disease. Transcriptomes were obtained from four E. coli backgrounds—AIEC16, LF82, Nissle 1917, and K‑12 C600—in both wild‑type (WT) and ΔargR mutant strains. Deletion of argR leads to constitutive upregulation of arginine biosynthesis genes, and this dataset supports comparative transcriptomic analyses aimed at identifying ArgR‑dependent regulatory networks. Differential expression analysis revealed that ArgR influences multiple virulence‑associated pathways in AIEC strains, including motility, invasion, biofilm formation, acid resistance, adhesion, lipopolysaccharide biosynthesis, and iron uptake. These RNA‑seq data provide a resource for exploring ArgR‑mediated transcriptional regulation and its contribution to AIEC pathogenicity.