Evidence map›Paper›PMID 27572649›Full record

ArticleNature microbiology2016

Persister formation in Staphylococcus aureus is associated with ATP depletion.

Brian P Conlon, Sarah E Rowe, Autumn Brown Gandt, Austin S Nuxoll, Niles P Donegan, Eliza A Zalis, Geremy Clair, Joshua N Adkins, Ambrose L Cheung, Kim Lewis

Abstract read
In one paragraph

Article in Nature microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 379 papers.

0numbers the graph read from it
0cells of the map it votes in
379citing papers in PubMed
–field-weighted citation impact
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

379 citing papers in PubMed.

  1. Dismantling the eDNA-mediated HBioactive materials · 2027
    Article
  2. Artificial intelligence catalyzes antimicrobial peptide design.Synthetic and systems biotechnology · 2027
    Review
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  10. Biofilm sensitization to breakJournal of medical microbiology · 2026
    Article
  11. Article
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  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

319 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Brian P ConlonAntimicrobial Discovery Center, Department of Biology, Northeastern University, Boston, Massachusetts 02115, USA.ORCID 0000-0002-2155-8375
Sarah E RoweAntimicrobial Discovery Center, Department of Biology, Northeastern University, Boston, Massachusetts 02115, USA.
Autumn Brown GandtAntimicrobial Discovery Center, Department of Biology, Northeastern University, Boston, Massachusetts 02115, USA.
Austin S NuxollAntimicrobial Discovery Center, Department of Biology, Northeastern University, Boston, Massachusetts 02115, USA.
Niles P DoneganDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire 03755, USA.ORCID 0000-0002-8328-2044
Eliza A ZalisAntimicrobial Discovery Center, Department of Biology, Northeastern University, Boston, Massachusetts 02115, USA.
Geremy ClairBiological Sciences Division, Pacific Northwest National Laboratory, Richland, Washington 99352, USA.
Joshua N AdkinsBiological Sciences Division, Pacific Northwest National Laboratory, Richland, Washington 99352, USA.ORCID 0000-0003-0399-0700
Ambrose L CheungDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire 03755, USA.
Kim LewisAntimicrobial Discovery Center, Department of Biology, Northeastern University, Boston, Massachusetts 02115, USA.

Funding

Developing therapeutics to treat chronic infectionsR01AI110578 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI LEE, RICHARD E., LEWIS, KIM · 2014 to 2018
$3.8M
NIAID NIH HHS R01 AI110578
6 · The paper itself

Abstract

Persisters are dormant phenotypic variants of bacterial cells that are tolerant to killing by antibiotics(1). Persisters are associated with chronic infections and antibiotic treatment failure(1-3). In Escherichia coli, toxin-antitoxin modules have been linked to persister formation(4-6). The mechanism of persister formation in Gram-positive bacteria is unknown. Staphylococcus aureus is a major human pathogen, responsible for a variety of chronic and relapsing infections such as osteomyelitis, endocarditis and infections of implanted devices. Deleting toxin-antitoxin modules in S. aureus did not affect the level of persisters. Here, we show that S. aureus persisters are produced due to a stochastic entrance into the stationary phase accompanied by a drop in intracellular adenosine triphosphate. Cells expressing stationary-state markers are present throughout the growth phase, and increase in frequency with cell density. Cell sorting revealed that the expression of stationary markers is associated with a 100-1,000-fold increase in the likelihood of survival to antibiotic challenge. The adenosine triphosphate level of the cell is predictive of bactericidal antibiotic efficacy and explains bacterial tolerance to antibiotics.

Indexed as

Adenosine TriphosphateAnti-Bacterial AgentsDrug ToleranceStaphylococcus aureusAdenosine TriphosphateAnti-Bacterial Agents

Identifiers

PMID27572649
PMCPMC4932909

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.