Evidence map›Paper›PMID 12533466›Full record

ArticleJournal of bacteriology2003

Heme-responsive transcriptional activation of Bordetella bhu genes.

Carin K Vanderpool, Sandra K Armstrong

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Contributions of the heme coordinating ligands of theThe Journal of biological chemistry · 2020
    Article
  6. Post-transcriptional regulation of theThe Journal of biological chemistry · 2019
    Article
  7. Article
  8. Article
  9. Iron homeostasis in theAdvances in botanical research · 2013
    Article
  10. Role and regulation of heme iron acquisition in gram-negative pathogens.Frontiers in cellular and infection microbiology · 2013
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Carin K VanderpoolDepartment of Microbiology, University of Minnesota Medical School, 420 Delaware Street S.E., Minneapolis, MN 55455-0312, USA.
Sandra K Armstrong
University of Minnesota Medical Center · US

Funding

IRON ACQUISITION IN BORDETELLA PERTUSSISR01AI031088 · NIAID · UNIVERSITY OF MINNESOTA TWIN CITIES · PI ARMSTRONG, SANDRA KAY · 1998 to 2014
$3.2M
MOLECULAR MECHANISMS OF INFECTIOUS DISEASE TRAININGT32AI007421 · NIAID · UNIVERSITY OF MINNESOTA TWIN CITIES · PI HAASE, ASHLEY T. · 1995 to 2004
$1.2M
NIAID NIH HHS R01 AI031088NIAID NIH HHS R01 AI 31088NIAID NIH HHS T32 AI007421NIAID NIH HHS T32 AI 07421
6 · The paper itself

Abstract

Bordetella pertussis and Bordetella bronchiseptica, gram-negative respiratory pathogens of mammals, possess a heme iron utilization system encoded by the bhuRSTUV genes. Preliminary evidence suggested that expression of the BhuR heme receptor was stimulated by the presence of heme under iron-limiting conditions. The hurIR (heme uptake regulator) genes were previously identified upstream of the bhuRSTUV gene cluster and are predicted to encode homologs of members of the iron starvation subfamily of extracytoplasmic function (ECF) regulators. In this study, B. pertussis and B. bronchiseptica DeltahurI mutants, predicted to lack an ECF sigma factor, were constructed and found to be deficient in the utilization of hemin and hemoglobin. Genetic complementation of DeltahurI strains with plasmid-borne hurI restored wild-type levels of heme utilization. B. bronchiseptica DeltahurI mutant BRM23 was defective in heme-responsive production of the BhuR heme receptor; hurI in trans restored heme-inducible BhuR expression to the mutant and resulted in BhuR overproduction. Transcriptional analyses with bhuR-lacZ fusion plasmids confirmed that bhuR transcription was activated in iron-starved cells in response to heme compounds. Heme-responsive bhuR transcription was not observed in mutant BRM23, indicating that hurI is required for positive regulation of bhu gene expression. Furthermore, bhuR was required for heme-inducible bhu gene activation, supporting the hypothesis that positive regulation of bhuRSTUV occurs by a surface signaling mechanism involving the heme-iron receptor BhuR.

Indexed as

Receptors, Cell SurfaceTranscriptional ActivationBacterial ProteinsBase SequenceBordetellaCulture MediaGenes, BacterialHemeIronMolecular Sequence DataMultigene FamilyMutationBacterial ProteinsBhuR protein, Bordetella pertussisCulture MediaHemeIronReceptors, Cell Surface

Identifiers

PMID12533466
PMCPMC142824
OpenAlexW2134365205

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.