Evidence map›Paper›PMID 19708918›Full record

ArticleMolecular microbiology2009

Symmetric signalling within asymmetric dimers of the Staphylococcus aureus receptor histidine kinase AgrC.

Elizabeth A George Cisar, Edward Geisinger, Tom W Muir, Richard P Novick

Abstract read
In one paragraph

Article in Molecular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed.

  1. Article
  2. EngineeredBiochemistry · 2026
    Article
  3. Molecular Mechanisms of Virulence Regulation inAccounts of chemical research · 2025
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Therapeutic Targeting of theFrontiers in microbiology · 2018
    Review
  13. Dynamic Modeling ofFrontiers in microbiology · 2018
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Elizabeth A George CisarLaboratory of Synthetic Protein Chemistry, Training Program in Chemical Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.Molecular Pathogenesis Program and Departments of Microbiology and Medicine, the Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA.
Edward GeisingerLaboratory of Synthetic Protein Chemistry, Training Program in Chemical Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.Molecular Pathogenesis Program and Departments of Microbiology and Medicine, the Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA.
Tom W MuirLaboratory of Synthetic Protein Chemistry, Training Program in Chemical Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.Molecular Pathogenesis Program and Departments of Microbiology and Medicine, the Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA.
Richard P NovickLaboratory of Synthetic Protein Chemistry, Training Program in Chemical Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.Molecular Pathogenesis Program and Departments of Microbiology and Medicine, the Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA.

Funding

PEPTIDE AUTOINDUCERS OF STAPHYLOCOCCAL PATHOGENICITYR01AI042783 · NIAID · PRINCETON UNIVERSITY · PI MUIR, TOM · 1998 to 2021
$7.9M
MOLECULAR GENETICS OF EXOTOXIN REGULATION IN S. AUREUSR01AI030138 · NIAID · PUBLIC HEALTH RESEARCH INSTITUTE · PI NOVICK, RICHARD P. · 1991 to 2011
$3.5M
NIAID NIH HHS R01 AI030138NIAID NIH HHS R01 AI042783NIAID NIH HHS R 501 AI42783
6 · The paper itself

Abstract

Virulence in Staphylococcus aureus is largely under control of the accessory gene regulator (agr) quorum-sensing system. The AgrC receptor histidine kinase detects its autoinducing peptide (AIP) ligand and generates an intracellular signal resulting in secretion of virulence factors. Although agr is a well-studied quorum-sensing system, little is known about the mechanism of AgrC activation. By co-immunoprecipitation analysis and intermolecular complementation of receptor mutants, we showed that AgrC forms ligand-independent dimers that undergo trans-autophosphorylation upon interaction with AIP. Remarkably, addition of specific AIPs to AgrC mutant dimers with only one functional sensor domain caused symmetric activation of either kinase domain despite the sensor asymmetry. Furthermore, mutant dimers involving one constitutive protomer demonstrated ligand-independent activity, irrespective of which protomer was kinase deficient. These results demonstrate that signalling through either individual AgrC protomer causes symmetric activation of both kinase domains. We suggest that such signalling across the dimer interface may be an important mechanism for dimeric quorum-sensing receptors to rapidly elicit a response upon signal detection.

Indexed as

Signal TransductionAmino Acid SequenceBacterial ProteinsGene Expression Regulation, BacterialGenetic Complementation TestMolecular Sequence DataPhosphorylationProtein KinasesProtein MultimerizationQuorum SensingSequence AlignmentStaphylococcus aureusVirulenceAgrC protein, StaphylococcusBacterial ProteinsProtein Kinases

Identifiers

PMID19708918
PMCPMC3913215

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.