Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Enterohemorrhagic Escherichia coli (EHEC)8624 double deletions of qseC and qseE grown in DMEM

ABSTRACT: Analysis of effect of deletion of the two adrenergic kinases QseC and QseE on gene expression of EHEC 8624 in the absence and presence of epinephrine A double mutant of qseC and qseE in the EHEC 8624 was grown in the absence or presence of epinephrine to OD600=1.0 in DMEM then processed according to manufacturer's specifications: http//www.affymetrix.com/support/technical/manual/expression_manual.affx

ORGANISM(S): Escherichia coli O157:H7

SUBMITTER: Jacqueline Njoroge

PROVIDER: E-GEOD-33895 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Enterohemorrhagic Escherichia coli virulence regulation by two bacterial adrenergic kinases, QseC and QseE.

Njoroge Jacqueline J Sperandio Vanessa V

Infection and immunity 20111205 2

The human pathogen enterohemorrhagic Escherichia coli (EHEC) O157:H7 has two histidine sensor kinases, QseC and QseE, which respond to the mammalian adrenergic hormones epinephrine and norepinephrine by increasing their autophosphorylation. Although QseC and QseE are present in nonpathogenic strains of E. coli, EHEC exploits these kinases for virulence regulation. To further investigate the full extent of epinephrine and its sensors' impact on EHEC virulence, we performed transcriptomic and phen ...[more]

PMID: 22144490

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Project description:The ability to respond to stress is at the core of an organismâs survival. The hormones epinephrine and norepinephrine play a central role in stress responses in mammals, which require the synchronized interaction of the whole neuroendocrine system. Bacteria also sense and respond to epinephrine and norepinephrine as a means to gauge the metabolic and immune state of the host. Mammalian adrenergic receptors are G-coupled protein receptors (GPCRs), bacteria, however, sense these hormones through histidine sensor kinases (HKs). HKs autophosphorylate in response to multiple signals and transfer this phosphate to response regulators (RRs). Two bacterial adrenergic receptors have been identified in EHEC, QseC and QseE, with QseE being downstream of QseC in this signaling cascade. We mapped the QseC signaling cascade in the deadly pathogen enterohemorrhagic E. coli (EHEC), which exploits this signaling system to promote disease. Through QseC, EHEC activates expression of metabolic, virulence and stress response genes, synchronizing the cell response to these stress hormones. Coordination of these responses is achieved by QseC phosphorylating three of the thirty two EHEC RRs. The QseB RR, which is QseCâs cognate RR, activates the flagella regulon which controls bacteria motility and chemotaxis. The QseF RR, which is phosphorylated by the QseE adrenergic sensor, coordinates expression of virulence genes involved in formation of lesions in the intestinal epithelia by EHEC, and the bacterial SOS stress response. The third RR, KdpE, controls potassium uptake, osmolarity response, and also the formation of lesions in the intestine. Adrenergic regulation of bacterial gene expression shares several parallels with mammalian adrenergic signaling having profound effects in the whole organism. Understanding adrenergic regulation of a bacterial cell is a powerful approach to study the underlying mechanisms of stress and cellular survival. Experiment Overall Design: Microarray comparisons reveal some trends with respect to signaling cascades. Comparative methods were used to identify networks.

Dataset Information

Enterohemorrhagic Escherichia coli (EHEC)8624 double deletions of qseC and qseE grown in DMEM

Publications

Enterohemorrhagic Escherichia coli virulence regulation by two bacterial adrenergic kinases, QseC and QseE.

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