The QseC adrenergic signaling cascade in enterohemorrhagic E. coli (EHEC)

David T. Hughes, Marcie B. Clarke, Kaneyoshi Yamamoto, David A. Rasko, Vanessa Sperandio

Research output: Contribution to journalArticle

121 Citations (Scopus)

Abstract

The ability to respond to stress is at the core of an organism's 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. Mammalian adrenergic receptors are G-coupled protein receptors (GPCRs); bacteria, however, sense these hormones through histidine sensor kinases (HKs). HKs autophosphorylate in response to 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. Here 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 QseC's cognate RR, activates the flagella regulon which controls bacteria motility and chemotaxis. The QseF RR, which is also 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, 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 for studying the underlying mechanisms of stress and cellular survival.

Original languageEnglish (US)
Article numbere1000553
JournalPLoS Pathogens
Volume5
Issue number8
DOIs
StatePublished - Aug 2009

Fingerprint

Enterohemorrhagic Escherichia coli
Adrenergic Agents
Hormones
Bacterial Gene Expression Regulation
Adrenergic Receptors
Virulence
Bacteria
Regulon
Neurosecretory Systems
Physiological Stress
Aptitude
Flagella
Chemotaxis
Intestinal Mucosa
G-Protein-Coupled Receptors
Osmolar Concentration
Epinephrine
Intestines
Mammals
Norepinephrine

ASJC Scopus subject areas

  • Microbiology
  • Parasitology
  • Virology
  • Immunology
  • Genetics
  • Molecular Biology

Cite this

The QseC adrenergic signaling cascade in enterohemorrhagic E. coli (EHEC). / Hughes, David T.; Clarke, Marcie B.; Yamamoto, Kaneyoshi; Rasko, David A.; Sperandio, Vanessa.

In: PLoS Pathogens, Vol. 5, No. 8, e1000553, 08.2009.

Research output: Contribution to journalArticle

Hughes, David T. ; Clarke, Marcie B. ; Yamamoto, Kaneyoshi ; Rasko, David A. ; Sperandio, Vanessa. / The QseC adrenergic signaling cascade in enterohemorrhagic E. coli (EHEC). In: PLoS Pathogens. 2009 ; Vol. 5, No. 8.
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