Evidence map›Paper›PMID 22174383›Full record

ArticleMicrobiology (Reading, England)2012

YgfZ contributes to secretion of cytotoxic necrotizing factor 1 into outer-membrane vesicles in Escherichia coli.

Hao Yu, Kwang Sik Kim

Abstract read
In one paragraph

Article in Microbiology (Reading, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Classification ofiScience · 2024
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Outer Membrane Vesicle Production byInternational journal of molecular sciences · 2021
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. 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 2 institutions in 1 country.

Hao YuDivision of Pediatric Infectious Diseases, Johns Hopkins University School of Medicine, 200 North Wolfe Street, Room 3157, Baltimore, MD 21287, USA.
Kwang Sik KimDivision of Pediatric Infectious Diseases, Johns Hopkins University School of Medicine, 200 North Wolfe Street, Room 3157, Baltimore, MD 21287, USA.
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

PATHOGENESIS OF NEONATAL MENINGITISR01NS026310 · NINDS · JOHNS HOPKINS UNIVERSITY · PI KIM, KWANG S · 1988 to 2008
$3.6M
E. coli invasion of brain endothelial cellsR56NS026310 · NINDS · JOHNS HOPKINS UNIVERSITY · PI KIM, KWANG S · 2009 to 2009
$410k
NINDS NIH HHS NS26310-22NINDS NIH HHS R01 NS026310NINDS NIH HHS R56 NS026310
6 · The paper itself

Abstract

Cytotoxic necrotizing factor 1 (CNF1), a Rho GTPase-activating bacterial toxin, has been shown to contribute to invasion by meningitis-causing Escherichia coli K1 of human brain microvascular endothelial cells (HBMEC), which constitute the blood-brain barrier. However, CNF1 is a cytosolic protein and it remains unclear how its secretion occurs, contributing to E. coli invasion of HBMEC. To investigate the genetic requirement for CNF1 secretion in E. coli K1 strain RS218, we performed mini-Tn5 in vitro mutagenesis and constructed a transposon mutant library of strain NBC, in which β-lactamase was fused to the C-terminus of CNF1 in the chromosome of strain RS218. We identified a transposon mutant (NBC-1E6) that exhibited reduced β-lactamase activity in its culture supernatant and had the transposon inserted into the ygfZ gene. When ygfZ was deleted from the genome of strain RS218 (ΔygfZ), the translocation of CNF1 into HBMEC was impaired. Subcellular localization analysis of CNF1 demonstrated that YgfZ, a periplasmic protein, contributes to secretion of CNF1 into outer-membrane vesicles (OMVs). The ΔygfZ mutant was significantly defective in invasion of HBMEC compared to the parent E. coli K1 strain. The defects of the ΔygfZ mutant in CNF1 secretion into OMVs and translocation into HBMEC as well as invasion of HBMEC were abrogated by complementation with ygfZ. Taken together, our findings demonstrate that YgfZ contributes to CNF1 secretion into OMVs in meningitis-causing E. coli K1.

Indexed as

Bacterial ToxinsCarrier ProteinsCells, CulturedDNA Transposable ElementsEndothelial CellsEscherichia coliEscherichia coli ProteinsExosomesGene DeletionHumansMutagenesis, InsertionalVirulence FactorsBacterial ToxinsCarrier Proteinscytotoxic necrotizing factor type 1DNA Transposable ElementsEscherichia coli ProteinsVirulence FactorsYgfZ protein, E coli

Identifiers

PMID22174383
PMCPMC3352114
OpenAlexW2144154113

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.