Evidence map›Paper›PMID 16672602›Full record

ArticleJournal of bacteriology2006

Signaling interactions between the aerotaxis transducer Aer and heterologous chemoreceptors in Escherichia coli.

Khoosheh K Gosink, Maria del Carmen Burón-Barral, John S Parkinson

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
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

40 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Signal integration in chemoreceptor complexes.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Article
  5. Article
  6. Conformational shifts in a chemoreceptor helical hairpin control kinase signaling inProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  7. Blue Light Is a Universal Signal forJournal of bacteriology · 2019
    Article
  8. Article
  9. Decoding the chemotactic signal.Journal of leukocyte biology · 2018
    Review
  10. Article
  11. A zipped-helix cap potentiates HAMP domain control of chemoreceptor signaling.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. The source of high signal cooperativity in bacterial chemosensory arrays.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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

3 authors at 1 institution in 1 country.

Khoosheh K GosinkBiology Department, University of Utah, Salt Lake City, 84112, USA.
Maria del Carmen Burón-Barral
John S Parkinson
University of Utah · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
Aerotactic Signaling by the Escherichia coli Aer ProteinR01GM062940 · NIGMS · UNIVERSITY OF UTAH · PI PARKINSON, JOHN S · 2001 to 2004
$750k
NCI NIH HHS CA42014NCI NIH HHS P30 CA042014NIGMS NIH HHS GM62940NIGMS NIH HHS R01 GM062940
6 · The paper itself

Abstract

Aer, a low-abundance signal transducer in Escherichia coli, mediates robust aerotactic behavior, possibly through interactions with methyl-accepting chemotaxis proteins (MCP). We obtained evidence for interactions between Aer and the high-abundance aspartate (Tar) and serine (Tsr) receptors. Aer molecules bearing a cysteine reporter diagnostic for trimer-of-dimer formation yielded cross-linking products upon treatment with a trifunctional maleimide reagent. Aer also formed mixed cross-linking products with a similarly marked Tar reporter. An Aer trimer contact mutation known to abolish trimer formation by MCPs eliminated Aer trimer and mixed trimer formation. Trimer contact alterations known to cause epistatic behavior in MCPs also produced epistatic properties in Aer. Amino acid replacements in the Tar trimer contact region suppressed an epistatic Aer signaling defect, consistent with compensatory conformational changes between directly interacting proteins. In cells lacking MCPs, Aer function required high-level expression, comparable to the aggregate number of receptors in a wild-type cell. Aer proteins with clockwise (CW)-biased signal output cannot function under these conditions but do so in the presence of MCPs, presumably through formation of mixed signaling teams. The Tar signaling domain was sufficient for functional rescue. Moreover, CW-biased lesions did not impair aerotactic signaling in a hybrid Aer-Tar transducer capable of adjusting its steady-state signal output via methylation-dependent sensory adaptation. Thus, MCPs most likely assist mutant Aer proteins to signal productively by forming collaborative signaling teams. Aer evidently evolved to operate collaboratively with high-abundance receptors but can also function without MCP assistance, provided that it can establish a suitable prestimulus swimming pattern.

Indexed as

Amino Acid SubstitutionBacterial ProteinsCarrier ProteinsChemoreceptor CellsEpistasis, GeneticEscherichia coliEscherichia coli ProteinsGene Expression Regulation, BacterialIntercellular Signaling Peptides and ProteinsMembrane ProteinsMutagenesis, Site-DirectedPlasmidsProtein ConformationSignal TransductionAer protein, E coliBacterial ProteinsCarrier ProteinsEscherichia coli ProteinsIntercellular Signaling Peptides and ProteinsMembrane Proteins

Identifiers

PMID16672602
PMCPMC1482851
OpenAlexW2128271995

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.