Evidence map›Paper›PMID 39883743›Full record

ArticlePLoS genetics2025

Tolerance mechanisms in polysaccharide biosynthesis: Implications for undecaprenol phosphate recycling in Escherichia coli and Shigella flexneri.

Jilong Qin, Yaoqin Hong, Nicholas T Maczuga, Renato Morona, Makrina Totsika

Abstract read
In one paragraph

Article in PLoS genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Functional loss ofFrontiers in microbiology · 2025
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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.

Jilong QinCentre for Immunology and Infection Control, School of Biomedical Sciences, Queensland University of Technology, Brisbane, QLD, Australia.ORCID https://orcid.org/0000-0002-5867-6332
Yaoqin HongCentre for Immunology and Infection Control, School of Biomedical Sciences, Queensland University of Technology, Brisbane, QLD, Australia.ORCID https://orcid.org/0000-0002-4408-2648
Nicholas T MaczugaSchool of Biological Sciences, Department of Molecular & Biomedical Sciences, Research Centre for Infectious Diseases, University of Adelaide, Adelaide, Australia.
Renato MoronaSchool of Biological Sciences, Department of Molecular & Biomedical Sciences, Research Centre for Infectious Diseases, University of Adelaide, Adelaide, Australia.
Makrina TotsikaCentre for Immunology and Infection Control, School of Biomedical Sciences, Queensland University of Technology, Brisbane, QLD, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bacterial polysaccharide synthesis is catalysed on the universal lipid carrier, undecaprenol phosphate (UndP). The cellular UndP pool is shared by different polysaccharide synthesis pathways including peptidoglycan biogenesis. Disruptions in cytosolic polysaccharide synthesis steps are detrimental to bacterial survival due to effects on UndP recycling. In contrast, bacteria can survive disruptions in the periplasmic steps, suggesting a tolerance mechanism to mitigate UndP sequestration. Here we investigated tolerance mechanisms to disruptions of polymerases that are involved in UndP-releasing steps in two related polysaccharide synthesis pathways: that for enterobacterial common antigen (ECA) and that for O antigen (OAg), in Escherichia coli and Shigella flexneri. Our study reveals that polysaccharide polymerisation is crucial for efficient UndP recycling. In E. coli K-12, cell survival upon disruptions in OAg polymerase is dependent on a functional ECA synthesis pathway and vice versa. This is because disruptions in OAg synthesis lead to the redirection of the shared lipid-linked sugar substrate UndPP-GlcNAc towards increased ECA production. Conversely, in S. flexneri, the OAg polymerase is essential due to its limited ECA production, which inadequately redirects UndP flow to support cell survival. We propose a model whereby sharing the initial sugar intermediate UndPP-GlcNAc between the ECA and OAg synthesis pathways allows UndP to be redirected towards ECA production, mitigating sequestration issues caused by disruptions in the OAg pathway. These findings suggest an evolutionary buffering mechanism that enhances bacterial survival when UndP sequestration occurs due to stalled polysaccharide biosynthesis, which may allow polysaccharide diversity in the species to increase over time.

Indexed as

Escherichia coliPolyisoprenyl PhosphatesPolysaccharides, BacterialShigella flexneriAntigens, BacterialO AntigensPolysaccharidesAntigens, Bacterialenterobacterial common antigenO AntigensPolyisoprenyl PhosphatesPolysaccharidesPolysaccharides, Bacterialundecaprenyl phosphate

Identifiers

PMID39883743
PMCPMC11813082

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Registered trials

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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.