Evidence map›Paper›PMID 30248093›Full record

ArticlePLoS genetics2018

A metabolic checkpoint protein GlmR is important for diverting carbon into peptidoglycan biosynthesis in Bacillus subtilis.

Vaidehi Patel, Qun Wu, Pete Chandrangsu, John D Helmann

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Staying in the loop to make ends meet: roles and regulation of GlmR inbioRxiv : the preprint server for biology · 2025
    Article
  4. Microbial Production ofFoods (Basel, Switzerland) · 2025
    Review
  5. Article
  6. Adaptation ofMicroorganisms · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Mutations inmBio · 2023
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 2 institutions in 2 countries.

Vaidehi PatelCornell University, Department of Microbiology, Ithaca, NY, United States of America.
Qun WuCornell University, Department of Microbiology, Ithaca, NY, United States of America.
Pete ChandrangsuCornell University, Department of Microbiology, Ithaca, NY, United States of America.ORCID 0000-0002-2601-7973
John D HelmannCornell University, Department of Microbiology, Ithaca, NY, United States of America.ORCID 0000-0002-3832-3249
Cornell University · USJiangnan University · CN

Funding

Bacillus subtilis Stress ResponsesR35GM122461 · NIGMS · CORNELL UNIVERSITY · PI John D Helmann · 2017 to 2026
$7.6M
NIGMS NIH HHS R35 GM122461
6 · The paper itself

Abstract

The Bacillus subtilis GlmR (formerly YvcK) protein is essential for growth on gluconeogenic carbon sources. Mutants lacking GlmR display a variety of phenotypes suggestive of impaired cell wall synthesis including antibiotic sensitivity, aberrant cell morphology and lysis. To define the role of GlmR, we selected suppressor mutations that ameliorate the sensitivity of a glmR null mutant to the beta-lactam antibiotic cefuroxime or restore growth on gluconeogenic carbon sources. Several of the resulting suppressors increase the expression of the GlmS and GlmM proteins that catalyze the first two committed steps in the diversion of carbon from central carbon metabolism into peptidoglycan biosynthesis. Chemical complementation studies indicate that the absence of GlmR can be overcome by provision of cells with N-acetylglucosamine (GlcNAc), even under conditions where GlcNAc cannot re-enter central metabolism and serve as a carbon source for growth. Our results indicate that GlmR facilitates the diversion of carbon from the central metabolite fructose-6-phosphate, which is limiting in cells growing on gluconeogenic carbon sources, into peptidoglycan biosynthesis. Our data suggest that GlmR stimulates GlmS activity, and we propose that this activation is antagonized by the known GlmR ligand and peptidoglycan intermediate UDP-GlcNAc. Thus, GlmR presides over a new mechanism for the regulation of carbon partitioning between central metabolism and peptidoglycan biosynthesis.

Indexed as

AcetylglucosamineAnti-Bacterial AgentsBacillus subtilisBacterial Proteinsbeta-Lactam ResistanceCarbohydrate MetabolismCell WallFructosephosphatesGene Expression Regulation, BacterialGlucoseMicrobial Sensitivity TestsMutationPeptidoglycanUridine Diphosphate N-AcetylglucosamineAcetylglucosamineAnti-Bacterial AgentsBacterial Proteinsfructose-6-phosphateFructosephosphatesGlucosePeptidoglycanUridine Diphosphate N-Acetylglucosamine

Identifiers

PMID30248093
PMCPMC6171935
OpenAlexW2892540384

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.