Transcriptional Profiling of an Attenuated Salmonella Typhimurium ptsI Mutant Strain Under Low-oxygen Conditions using Microarray Analysis.
10.4167/jbv.2015.45.3.200
- Author:
Sangyong LIM
1
;
Ahreum HAN
;
Dongho KIM
;
Ho Seong SEO
Author Information
1. Research Division for Biotechnology, Korea Atomic Energy Research Institute, Jeongeup, Korea. hoseongseo@kaeri.re.kr
- Publication Type:Original Article
- Keywords:
Salmonella Typhimurium;
PTS;
Flagella;
Invasion
- MeSH:
Animals;
Diarrhea;
Flagella;
Humans;
Metabolism;
Mice;
Microarray Analysis*;
Oligonucleotide Array Sequence Analysis;
Phosphoenolpyruvate;
Salmonella typhimurium*;
Salmonella*;
Serine;
Threonine;
Typhoid Fever;
Virulence
- From:Journal of Bacteriology and Virology
2015;45(3):200-214
- CountryRepublic of Korea
- Language:English
-
Abstract:
Salmonella causes a wide variety of diseases ranging from mild diarrhea to severe systemic infections, such as like typhoid fever, in multiple organisms, ranging from mice to humans. A lack of ptsI, which encodes the first component of phosphoenolpyruvate (PEP) : carbohydrate phosphotransferase system (PTS), is known to cause Salmonella Typhimurium attenuation; however, the mechanisms behind this have not yet been elucidated. In this study, a DNA microarray was performed to determine why the virulence of ptsI mutants is attenuated under low-oxygen conditions in which the ptsI expression is enhanced. Of 106 down-regulated genes, the most repressed were pdu and tdc genes, which are required for propanediol utilization and threonine and serine metabolism, respectively. In addition, half the flagellar genes were down-regulated in the ptsI mutant strain. Because pdu genes are induced during infection and Tdc products and flagella-mediated motility are necessary for the invasion of S. Typhimurium, the invasive ability of ptsI mutants was examined. We found that ptsI mutation reduced the ability of S. Typhimurium to invade into host cells, suggesting that reduced expression of the pdu, tdc, and flagellar genes is involved in the attenuation of ptsI mutants.
