Evidence map›Paper›PMID 18599839›Full record

ArticleMicrobiology (Reading, England)2008

ClpXP proteases positively regulate alginate overexpression and mucoid conversion in Pseudomonas aeruginosa.

Dongru Qiu, Vonya M Eisinger, Nathan E Head, Gerald B Pier, Hongwei D Yu

Open access · greenAbstract read
In one paragraph

Article in Microbiology (Reading, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing 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

59 citing papers in PubMed, 103 citations in OpenAlex.

  1. Trial
  2. Article
  3. ClpP2 modulates ClpXP assembly to promote multiple pathogenic phenotypes inProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Advances in alginate biosynthesis: regulation and production inFrontiers in bioengineering and biotechnology · 2025
    Review
  5. Journal of bacteriology · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. LeveragingFrontiers in microbiology · 2021
    Review
  18. Review
  19. Article
  20. ClpP Protease, a Promising Antimicrobial Target.International journal of molecular sciences · 2019
    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

5 authors at 2 institutions in 1 country.

Dongru QiuDepartment of Biochemistry and Microbiology, Joan C. Edwards School of Medicine at Marshall University, Huntington, WV 25755-9320, USA.
Vonya M EisingerDepartment of Biochemistry and Microbiology, Joan C. Edwards School of Medicine at Marshall University, Huntington, WV 25755-9320, USA.
Nathan E HeadDepartment of Biochemistry and Microbiology, Joan C. Edwards School of Medicine at Marshall University, Huntington, WV 25755-9320, USA.
Gerald B PierChanning Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Hongwei D YuDepartment of Pediatrics, Joan C. Edwards School of Medicine at Marshall University, Huntington, WV 25701-3655, USA.
Marshall University · USBrigham and Women's Hospital · US

Funding

VIRULENCE AND IMMUNITY TO MUCOID P. AERUGINOSAR01AI048917 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI PIER, GERALD B · 2001 to 2009
$3.2M
NIAID NIH HHS AI 48917-04NIAID NIH HHS R01 AI048917
6 · The paper itself

Abstract

Overproduction of the exopolysaccharide alginate and conversion to a mucoid phenotype in Pseudomonas aeruginosa are markers for the onset of chronic lung infection in cystic fibrosis (CF). Alginate production is regulated by the extracytoplasmic function (ECF) sigma factor AlgU/T and the cognate anti-sigma factor MucA. Many clinical mucoid isolates carry loss-of-function mutations in mucA. These mutations, including the most common mucA22 allele, cause C-terminal truncations in MucA, indicating that an inability to regulate AlgU activity by MucA is associated with conversion to the mucoid phenotype. Here we report that a mutation in a stable mucoid strain derived from the parental strain PAO1, designated PAO581, that does not contain the mucA22 allele, was due to a single-base deletion in mucA (DeltaT180), generating another type of C-terminal truncation. A global mariner transposon screen in PAO581 for non-mucoid isolates led to the identification of three regulators of alginate production, clpP (PA1801), clpX (PA1802), and a clpP paralogue (PA3326, designated clpP2). The PAO581 null mutants of clpP, clpX and clpP2 showed decreased AlgU transcriptional activity and an accumulation of haemagglutinin (HA)-tagged N-terminal MucA protein with an apparent molecular mass of 15 kDa. The clpP and clpX mutants of a CF mucoid isolate revert to the non-mucoid phenotype. The ClpXP and ClpP2 proteins appear to be part of a proteolytic network that degrades the cytoplasmic portion of truncated MucA proteins to release the sequestered AlgU, which drives alginate biosynthesis.

Indexed as

Gene Expression Regulation, BacterialAlginatesBacterial ProteinsCystic FibrosisGlucuronic AcidGlycosaminoglycansHexuronic AcidsHumansMolecular Sequence DataMutagenesis, InsertionalPeptide HydrolasesPhenotypePoint MutationPseudomonas aeruginosaPseudomonas InfectionsSigma FactorAlginatesAlgU protein, Pseudomonas aeruginosaBacterial ProteinsGlucuronic AcidGlycosaminoglycansHexuronic AcidsMucA protein, Pseudomonasmucoid exopolysaccharide (P aeruginosa)Peptide HydrolasesSigma Factor

Identifiers

PMID18599839
PMCPMC2995304
OpenAlexW1985692996

What OpenQuestion holds

Textmetadata
LicenceTDM
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.