Evidence map›Paper›PMID 30964003›Full record

ArticleeLife2019

A switch in surface polymer biogenesis triggers growth-phase-dependent and antibiotic-induced bacteriolysis.

Josué Flores-Kim, Genevieve S Dobihal, Andrew Fenton, David Z Rudner, Thomas G Bernhardt

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. mBio · 2026
    Article
  3. Article
  4. Review
  5. bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. CombattingAntibiotics (Basel, Switzerland) · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. A periplasmic protein modulates the proteolysis of peptidoglycan hydrolases to maintain cell wall homeostasis inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 1 institution in 2 countries.

Josué Flores-KimDepartment of Microbiology, Harvard Medical School, Boston, United States.ORCID 0000-0001-8282-6647
Genevieve S DobihalDepartment of Microbiology, Harvard Medical School, Boston, United States.
Andrew FentonDepartment of Microbiology, Harvard Medical School, Boston, United States.
David Z RudnerDepartment of Microbiology, Harvard Medical School, Boston, United States.ORCID 0000-0002-0236-7143
Thomas G BernhardtDepartment of Microbiology, Harvard Medical School, Boston, United States.ORCID 0000-0003-3566-7756
Boston University · US

Funding

Targeting bacterial cell wall biogenesis for the development of novel antimicrobU19AI109764 · NIAID · HARVARD MEDICAL SCHOOL · PI BELTZ, GERALD A · 2014 to 2018
$25.2M
Peptidoglycan Biogenesis in Escherichia ColiR01AI083365 · NIAID · HARVARD MEDICAL SCHOOL · PI Thomas G Bernhardt · 2010 to 2026
$8.3M
Membrane Remodeling and Protein Trafficking in BacteriaR01GM073831 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI RUDNER, DAVID Z · 2005 to 2014
$3.4M
Cell surface biogenesis in Streptococcus pneumoniaeR01AI139083 · NIAID · HARVARD MEDICAL SCHOOL · PI RUDNER, DAVID Z · 2019 to 2023
$2.2M
A multidisciplinary approach to elucidating gene function in a model Gram-positivRC2GM092616 · NIGMS · HARVARD MEDICAL SCHOOL · PI RUDNER, DAVID Z · 2009 to 2010
$2.0M
Cell Envelope Homeostasis in Bacillus subtilisR01GM127399 · NIGMS · HARVARD MEDICAL SCHOOL · PI RUDNER, DAVID Z · 2019 to 2022
$1.4M
Elucidating novel mechanisms controlling cell envelope biogenesis in Streptococcus PneumoniaeF32AI136431 · NIAID · HARVARD MEDICAL SCHOOL · PI FLORES-KIM, JOSUE · 2018 to 2020
$192k
NIAID NIH HHS F32 AI136431NIAID NIH HHS R01 AI083365NIAID NIH HHS R01 AI139083NIAID NIH HHS U19 AI109764NIGMS NIH HHS R01 GM073831NIGMS NIH HHS R01 GM127399NIGMS NIH HHS RC2 GM092616NIH HHS F32AI36431NIH HHS R01AI139083
6 · The paper itself

Abstract

Penicillin and related antibiotics disrupt cell wall synthesis to induce bacteriolysis. Lysis in response to these drugs requires the activity of cell wall hydrolases called autolysins, but how penicillins misactivate these deadly enzymes has long remained unclear. Here, we show that alterations in surface polymers called teichoic acids (TAs) play a key role in penicillin-induced lysis of the Gram-positive pathogen

Indexed as

Anti-Bacterial AgentsBacteriolysisBiosynthetic PathwaysPenicillinsStreptococcus pneumoniaeTeichoic AcidsAnti-Bacterial AgentsPenicillinsTeichoic Acidsantibioticscell wallinfectious diseasemicrobiologypeptidoglycanS. pneumoniaeteichoic acid

Identifiers

PMID30964003
PMCPMC6456293
OpenAlexW2940289922

What OpenQuestion holds

Textmetadata
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.