Expression analysis of Escherichia coli CC72 before and after osmotic stress
Ontology highlight
ABSTRACT:
ORGANISM(S): Escherichia coli K-12 Escherichia coli str. K-12 substr. MG1655
PROVIDER: GSE110730 | GEO | 2018/04/11
REPOSITORIES: GEO
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Project description:A transcription factor (TF), OmpR, plays a critical role in transcriptional regulation of the defense system for osmotic stress in bacteria. However, its full genome-wide regulatory potential is unknown. Here, we perform a genome-scale reconstruction of the OmpR regulon in Escherichia coli K-12 MG1655. Integrative data analysis reveals that a total of 37 genes in 24 transcription units (TUs) belong to OmpR regulon. Among them, 26 genes show more than two-fold changes in expression level under OmpR knock-out condition. We find that OmpR tends to regulate mostly membrane-located gene products of diverse fundamental biological processes, such as narU, ompX, and nuoN. Investigating co-regulation of entire set of genes regulated by other stress-response TFs unveils that they are surprisingly independently regulated by TF(s) responding to each stress. Additionally, detailed investigation of physiological roles of newly discovered OmpR regulon reveals that activation of narU encoding nitrate/nitrite transporter is a relatively unique strategy of E. coli K-12 MG1655 to significantly improve cellular tolerance toward osmotic stress.
2017-06-09 | GSE88980 | GEO
Project description:A transcription factor (TF), OmpR, plays a critical role in transcriptional regulation of the defense system for osmotic stress in bacteria. However, its full genome-wide regulatory potential is unknown. Here, we perform a genome-scale reconstruction of the OmpR regulon in Escherichia coli K-12 MG1655. Integrative data analysis reveals that a total of 37 genes in 24 transcription units (TUs) belong to OmpR regulon. Among them, 26 genes show more than two-fold changes in expression level under OmpR knock-out condition. We find that OmpR tends to regulate mostly membrane-located gene products of diverse fundamental biological processes, such as narU, ompX, and nuoN. Investigating co-regulation of entire set of genes regulated by other stress-response TFs unveils that they are surprisingly independently regulated by TF(s) responding to each stress. Additionally, detailed investigation of physiological roles of newly discovered OmpR regulon reveals that activation of narU encoding nitrate/nitrite transporter is a relatively unique strategy of E. coli K-12 MG1655 to significantly improve cellular tolerance toward osmotic stress.
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Project description:Escherichia coli O157 presents a number of specific problems in terms of food safety and public health. It has been found that E. coli O157 is more resistant to a number of the stresses encountered during food production such as heat, pH and osmotic shock. This greater resistance is thought to contribute to the low infectious dose of E. coli O157 (<100 organisms). Moreover, E. coli O157 is associated with debilitating conditions such as haemorrhagic colitis and haemoytic uraemic syndrome, particularly in children and the elderly. We have been studying the stress responses of E. coli O157:H7 (Sakai) and comparing with a commensal strain of E. coli K-12, MG1655. We found that E. coli O157 (Sakai) is more sensitive to oxidative stress than MG1655. A microarray study of these strains treated with sub-lethal concentrations (0.5mg/ml) of menadione revealed big differences in their responses. In E. coli O157 (Sakai), 540 genes responded significantly to the treatment compared to 121 genes in MG1655. One surprising finding from the microarray data was the observation that many iron-transport genes were up-regulated in E. coli O157 (Sakai) whereas relatively few were induced in MG1655 despite the fact that the bacteria were grown in a medium containing ample iron. We speculated that the induction of iron transport genes in an iron-rich medium might have contributed to the enhanced killing of E. coli O157 (Sakai) through triggering of a Fenton reaction. We speculated that the difference in sensitivity to oxidative stress might be due to differences in the intracellular iron content of E. coli O157 and MG1655. We found that E. coli O157 contains ~50% more iron than MG1655 and believe that during oxidative stress, this iron is released by damaged proteins. The greater levels of free iron in E. coli O157 will trigger a greater Fenton reaction that can damage the ferric uptake regulator (Fur), resulting in unregulated iron transport. In MG1655, the lower iron content results in a smaller Fenton reaction, enabling the cellular protection systems to limit damage and protect Fur.
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