The transcription factor SlyA from Salmonella Typhimurium regulates genes in response to hydrogen peroxide and sodium hypochlorite

Carolina E. Cabezas, Alan C. Briones, Camila Aguirre, Coral Pardo-Esté, Juan Castro-Severyn, César R. Salinas, María S. Baquedano, Alejandro A. Hidalgo, Juan A. Fuentes, Eduardo H. Morales, Claudio A. Meneses, Eduardo Castro-Nallar, Claudia Paz Saavedra*

*Autor corresponent d’aquest treball

Producció científica: Article en revista indexadaArticleAvaluat per experts

18 Cites (Scopus)

Resum

Salmonella Typhimurium is an intracellular pathogen that is capable of generating systemic fever in a murine model. Over the course of the infection, Salmonella faces different kinds of stressors, including harmful reactive oxygen species (ROS). Various defence mechanisms enable Salmonella to successfully complete the infective process in the presence of such stressors. The transcriptional factor SlyA is involved in the oxidative stress response and invasion of murine macrophages. We evaluated the role of SlyA in response to H2O2 and NaOCl and found an increase of slyA expression upon exposure to these toxics. However, the SlyA target genes and the molecular mechanisms by which they influence the infective process are unknown. We hypothesised that SlyA regulates the expression of genes required for ROS resistance, metabolism, or virulence under oxidative stress conditions. Transcriptional profiling in wild type and ΔslyA strains confirmed that SlyA regulates the expression of several genes involved in virulence [sopD (STM14_3550), sopE2 (STM14_2244), hilA (STM14_3475)] and central metabolism [kgtP (STM14_3252), fruK (STM14_2722), glpA (STM14_2819)] in response to H2O2 and NaOCl. These findings were corroborated by functional assay and transcriptional fusion assays using GFP. DNA-protein interaction assays showed that SlyA regulates these genes through direct interaction with their promoter regions.

Idioma originalAnglès
Pàgines (de-a)263-278
Nombre de pàgines16
RevistaResearch in Microbiology
Volum169
Número6
DOIs
Estat de la publicacióPublicada - 1 de jul. 2018
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