Evidence map›Paper›PMID 26593043›Full record

ArticleMolecular microbiology2016

Dead-end intermediates in the enterobacterial common antigen pathway induce morphological defects in Escherichia coli by competing for undecaprenyl phosphate.

Matthew A Jorgenson, Suresh Kannan, Mary E Laubacher, Kevin D Young

Open access · bronzeAbstract read
In one paragraph

Article in Molecular microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

83 citing papers in PubMed, 135 citations in OpenAlex.

  1. Article
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  5. Bacteriophages target membrane-anchored glycopolymers to promote host cell lysis and progeny release.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  6. Stepwise Assembly of theBiochemistry · 2026
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  7. Review
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  9. Dysregulation of a nucleotidyltransferase induces division and surface glycan defects inProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  10. Article
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  12. Journal of bacteriology · 2025
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  13. Article
  14. Functional loss ofFrontiers in microbiology · 2025
    Article
  15. Article
  16. Article
  17. Review
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  20. Review

23 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Matthew A JorgensonDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA.
Suresh KannanDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA.
Mary E LaubacherDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA.
Kevin D YoungDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA.ORCID http://orcid.org/0000-0003-1760-281X
University of Arkansas for Medical Sciences · US

Funding

Glycan Expression Analysis using an Odyssey CLx Infrared Imaging SystemR01GM061019 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI VOTH, DANIEL E · 2000 to 2021
$8.0M
NIGMS NIH HHS GM061019NIGMS NIH HHS R01 GM061019
6 · The paper itself

Abstract

Bacterial morphology is determined primarily by the architecture of the peptidoglycan (PG) cell wall, a mesh-like layer that encases the cell. To identify novel mechanisms that create or maintain cell shape in Escherichia coli, we used flow cytometry to screen a transposon insertion library and identified a wecE mutant that altered cell shape, causing cells to filament and swell. WecE is a sugar aminotransferase involved in the biosynthesis of enterobacterial common antigen (ECA), a non-essential outer membrane glycolipid of the Enterobacteriaceae. Loss of wecE interrupts biosynthesis of ECA and causes the accumulation of the undecaprenyl pyrophosphate-linked intermediate ECA-lipid II. The wecE shape defects were reversed by: (i) preventing initiation of ECA biosynthesis, (ii) increasing the synthesis of the lipid carrier undecaprenyl phosphate (Und-P), (iii) diverting Und-P to PG synthesis or (iv) promoting Und-P recycling. The results argue that the buildup of ECA-lipid II sequesters part of the pool of Und-P, which, in turn, adversely affects PG synthesis. The data strongly suggest there is competition for a common pool of Und-P, whose proper distribution to alternate metabolic pathways is required to maintain normal cell shape in E. coli.

Indexed as

Metabolic Networks and PathwaysAntigens, BacterialCell WallEscherichia coliEscherichia coli ProteinsGene Expression Regulation, BacterialGenotypeMutationPolyisoprenyl PhosphatesTransaminasesUridine Diphosphate N-Acetylmuramic AcidAntigens, Bacterialenterobacterial common antigenEscherichia coli Proteinsmuramyl-NAc-(pentapeptide)pyrophosphoryl-undecaprenolPolyisoprenyl PhosphatesTransaminasesundecaprenyl phosphateUridine Diphosphate N-Acetylmuramic AcidWecE protein, E coli

Identifiers

PMID26593043
PMCPMC4845916
OpenAlexW2174282801

What OpenQuestion holds

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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.