Evidence map›Paper›PMID 21685290›Full record

ArticleJournal of bacteriology2011

The requirement for pneumococcal MreC and MreD is relieved by inactivation of the gene encoding PBP1a.

Adrian D Land, Malcolm E Winkler

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Analysis of essential genes inJournal of bacteriology · 2025
    Article
  3. Article
  4. Analysis of Essential Genes inbioRxiv : the preprint server for biology · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Characterization of MreCD inJournal of oral microbiology · 2025
    Article
  9. Article
  10. Elongasome core proteins and class A PBP1a display zonal, processive movement at the midcell ofProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

8 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

2 authors at 1 institution in 1 country.

Adrian D LandDepartment of Biology, Indiana University Bloomington, 1001 East Third Street, Bloomington, IN 47405, USA.
Malcolm E Winkler
Indiana University Bloomington · US

Funding

TRAINING IN GENETICST32GM007757 · NIGMS · TRUSTEES OF INDIANA UNIVERSITY · PI KUMAR, JUSTIN P · 1985 to 2014
$8.1M
Signal Transduction by Essential VicRKX in PneumococcusR01AI060744 · NIAID · TRUSTEES OF INDIANA UNIVERSITY · PI WINKLER, MALCOLM E. · 2006 to 2010
$1.8M
Global Genetic Interaction Profiling in ProkaryotesR01GM085697 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GROSS, CAROL ANNE · 2008 to 2011
$1.6M
NIAID NIH HHS R01 AI060744NIAID NIH HHS R01AI060744NIGMS NIH HHS R01 GM085697NIGMS NIH HHS T32 GM007757NIGMS NIH HHS T32GM007757
6 · The paper itself

Abstract

MreC and MreD, along with the actin homologue MreB, are required to maintain the shape of rod-shaped bacteria. The depletion of MreCD in rod-shaped bacteria leads to the formation of spherical cells and the accumulation of suppressor mutations. Ovococcus bacteria, such as Streptococcus pneumoniae, lack MreB homologues, and the functions of the S. pneumoniae MreCD (MreCD(Spn)) proteins are unknown. mreCD are located upstream from the pcsB cell division gene in most Streptococcus species, but we found that mreCD and pcsB are transcribed independently. Similarly to rod-shaped bacteria, we show that mreCD are essential in the virulent serotype 2 D39 strain of S. pneumoniae, and the depletion of MreCD results in cell rounding and lysis. In contrast, laboratory strain R6 contains suppressors that allow the growth of ΔmreCD mutants, and bypass suppressors accumulate in D39 ΔmreCD mutants. One class of suppressors eliminates the function of class A penicillin binding protein 1a (PBP1a). Unencapsulated Δpbp1a D39 mutants have smaller diameters than their pbp1a(+) parent or Δpbp2a and Δpbp1b mutants, which lack other class A PBPs and do not show the suppression of ΔmreCD mutations. Suppressed ΔmreCD Δpbp1a double mutants form aberrantly shaped cells, some with misplaced peptidoglycan (PG) biosynthesis compared to that of single Δpbp1a mutants. Quantitative Western blotting showed that MreC(Spn) is abundant (≈8,500 dimers per cell), and immunofluorescent microscopy (IFM) located MreCD(Spn) to the equators and septa of dividing cells, similarly to the PBPs and PG pentapeptides indicative of PG synthesis. These combined results are consistent with a model in which MreCD(Spn) direct peripheral PG synthesis and control PBP1a localization or activity.

Indexed as

Bacterial ProteinsGene DeletionGene Expression Regulation, BacterialPeptidyl TransferasesStreptococcus pneumoniaeBacterial ProteinsMreC protein, BacteriaPBP1a protein, Streptococcus pneumoniaePeptidyl Transferases

Identifiers

PMID21685290
PMCPMC3147673
OpenAlexW2151395519

What OpenQuestion holds

Textmetadata
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.