Evidence map›Paper›PMID 36218368›Full record

ArticlemBio2022

Metabolic Mechanism and Physiological Role of Glycerol 3-Phosphate in Pseudomonas aeruginosa PAO1.

Yidong Liu, Wenxuan Sun, Liting Ma, Rong Xu, Chunyu Yang, Ping Xu, Cuiqing Ma, Chao Gao

Open access · goldAbstract read
In one paragraph

Article in mBio, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  3. Predicting Strain-Specific Metabolic Capabilities in the GenusComputational and structural biotechnology journal · 2026
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  7. Epigenetic cellular memory inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Metabolic response of Klebsiella oxytoca to ciprofloxacin exposure: a metabolomics approach.Metabolomics : Official journal of the Metabolomic Society · 2024
    Article
  13. Article
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

8 authors at 3 institutions in 1 country.

Yidong LiuState Key Laboratory of Microbial Technology, Shandong University, Qingdao, People's Republic of China.
Wenxuan SunState Key Laboratory of Microbial Technology, Shandong University, Qingdao, People's Republic of China.
Liting MaState Key Laboratory of Microbial Technology, Shandong University, Qingdao, People's Republic of China.
Rong XuState Key Laboratory of Microbial Technology, Shandong University, Qingdao, People's Republic of China.
Chunyu YangState Key Laboratory of Microbial Technology, Shandong University, Qingdao, People's Republic of China.
Ping XuState Key Laboratory of Microbial Metabolism, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Cuiqing MaState Key Laboratory of Microbial Technology, Shandong University, Qingdao, People's Republic of China.
Chao GaoState Key Laboratory of Microbial Technology, Shandong University, Qingdao, People's Republic of China.
Shandong University · CNShanghai Jiao Tong University · CNState Key Laboratory of Microbial Technology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudomonas aeruginosa is an important opportunistic pathogen that is lethal to cystic fibrosis (CF) patients. Glycerol generated during the degradation of phosphatidylcholine, the major lung surfactant in CF patients, could be utilized by P. aeruginosa. Previous studies have indicated that metabolism of glycerol by this bacterium contributes to its adaptation to and persistence in the CF lung environment. Here, we investigated the metabolic mechanisms of glycerol and its important metabolic intermediate glycerol 3-phosphate (G3P) in P. aeruginosa PAO1. We found that G3P homeostasis plays an important role in the growth and virulence factor production of P. aeruginosa PAO1. The G3P accumulation caused by the mutation of G3P dehydrogenase (GlpD) and exogenous glycerol led to impaired growth and reductions in pyocyanin synthesis, motilities, tolerance to oxidative stress, and resistance to kanamycin. Transcriptomic analysis indicates that the growth retardation caused by G3P stress is associated with reduced glycolysis and adenosine triphosphate (ATP) generation. Furthermore, two haloacid dehalogenase-like phosphatases (PA0562 and PA3172) that play roles in the dephosphorylation of G3P in strain PAO1 were identified, and their enzymatic properties were characterized. Our findings reveal the importance of G3P homeostasis and indicate that GlpD, the key enzyme for G3P catabolism, is a potential therapeutic target for the prevention and treatment of infections by this pathogen.

Indexed as

Cystic FibrosisPseudomonas InfectionsAnti-Bacterial AgentsGlycerolGlycerophosphatesHumansKanamycinOxidoreductasesPseudomonas aeruginosaVirulence Factorsalpha-glycerophosphoric acidAnti-Bacterial AgentsGlycerolGlycerophosphatesKanamycinOxidoreductasesVirulence Factorsglycerolglycerol 3-phosphateglycerol 3-phosphate dehydrogenaseglycerol 3-phosphate phosphatasePseudomonas aeruginosa

Identifiers

PMID36218368
PMCPMC9765544
OpenAlexW4304191926

What OpenQuestion holds

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LicenceCC BY
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.