Evidence map›Paper›PMID 23935043›Full record

ArticleJournal of bacteriology2013

Staphylococcus aureus mutants lacking the LytR-CpsA-Psr family of enzymes release cell wall teichoic acids into the extracellular medium.

Yvonne G Y Chan, Matthew B Frankel, Vanina Dengler, Olaf Schneewind, Dominique Missiakas

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bacteriology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
5.8field-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

75 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. ThemBio · 2025
    Article
  7. Review
  8. Article
  9. A novel polysaccharide in the envelope ofJournal of bacteriology · 2025
    Article
  10. Review
  11. Article
  12. The roles of GpsB and DivIVA inFrontiers in microbiology · 2023
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. d-Alanylation of Lipoteichoic Acids inFrontiers in microbiology · 2022
    Article
  20. Article

15 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

5 authors at 3 institutions in 2 countries.

Yvonne G Y ChanDepartment of Microbiology, University of Chicago, Chicago, Illinois, USA.
Matthew B Frankel
Vanina Dengler
Olaf Schneewind
Dominique Missiakas
Argonne National Laboratory · USUniversity of Chicago · USUniversity of Zurich · CH

Funding

Vaccines and Therapies Against BotulismU54AI057153 · NIAID · UNIVERSITY OF CHICAGO · PI KAWAOKA, YOSHIHIRO · 2003 to 2013
$87.6M
Surface Proteins of Gram-Positive BacteriaR01AI038897 · NIAID · UNIVERSITY OF CHICAGO · PI MISSIAKAS, DOMINIQUE M. · 1996 to 2024
$8.9M
NIAID NIH HHS 1-U54-AI-057153NIAID NIH HHS R01 AI038897NIAID NIH HHS R01 AI38897NIAID NIH HHS U54 AI057153
6 · The paper itself

Abstract

The LytR-CpsA-Psr (LCP) proteins are thought to transfer bactoprenol-linked biosynthetic intermediates of wall teichoic acid (WTA) to the peptidoglycan of Gram-positive bacteria. In Bacillus subtilis, mutants lacking all three LCP enzymes do not deposit WTA in the envelope, while Staphylococcus aureus Δlcp mutants display impaired growth and reduced levels of envelope phosphate. We show here that the S. aureus Δlcp mutant synthesized WTA yet released ribitol phosphate polymers into the extracellular medium. Further, Δlcp mutant staphylococci no longer restricted the deposition of LysM-type murein hydrolases to cell division sites, which was associated with defects in cell shape and increased autolysis. Mutations in S. aureus WTA synthesis genes (tagB, tarF, or tarJ2) inhibit growth, which is attributed to the depletion of bactoprenol, an essential component of peptidoglycan synthesis (lipid II). The growth defect of S. aureus tagB and tarFJ mutants was alleviated by inhibition of WTA synthesis with tunicamycin, whereas the growth defect of the Δlcp mutant was not relieved by tunicamycin treatment or by mutation of tagO, whose product catalyzes the first committed step of WTA synthesis. Further, sortase A-mediated anchoring of proteins to peptidoglycan, which also involves bactoprenol and lipid II, was not impaired in the Δlcp mutant. We propose a model whereby the S. aureus Δlcp mutant, defective in tethering WTA to the cell wall, cleaves WTA synthesis intermediates, releasing ribitol phosphate into the medium and recycling bactoprenol for peptidoglycan synthesis.

Indexed as

Cell DivisionCell MembraneCell WallCulture MediaGene Expression Regulation, BacterialGene Expression Regulation, EnzymologicMultigene FamilyMutationStaphylococcus aureusTeichoic AcidsCulture MediaTeichoic Acids

Identifiers

PMID23935043
PMCPMC3807444
OpenAlexW2018479585

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.