Evidence map›Paper›PMID 29572241›Full record

ArticleThe EMBO journal2018

Contact-dependent growth inhibition induces high levels of antibiotic-tolerant persister cells in clonal bacterial populations.

Anirban Ghosh, Özden Baltekin, Marcus Wäneskog, Dina Elkhalifa, Disa L Hammarlöf, Johan Elf, Sanna Koskiniemi

Abstract read
In one paragraph

Article in The EMBO journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Microbial genomics · 2021
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Contact-Dependent Growth Inhibition in Bacteria: Do Not Get Too Close!International journal of molecular sciences · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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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

7 authors.

Anirban GhoshDepartment of Cell and Molecular Biology, Uppsala University, Uppsala, Sweden.
Özden BaltekinDepartment of Cell and Molecular Biology, Uppsala University, Uppsala, Sweden.
Marcus WäneskogDepartment of Cell and Molecular Biology, Uppsala University, Uppsala, Sweden.
Dina ElkhalifaDepartment of Cell and Molecular Biology, Uppsala University, Uppsala, Sweden.
Disa L HammarlöfDepartment of Cell and Molecular Biology, Uppsala University, Uppsala, Sweden.
Johan ElfDepartment of Cell and Molecular Biology, Uppsala University, Uppsala, Sweden.ORCID 0000-0001-5522-1810
Sanna KoskiniemiDepartment of Cell and Molecular Biology, Uppsala University, Uppsala, Sweden sanna.koskiniemi@icm.uu.se.ORCID 0000-0002-3275-0936

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bacterial populations can use bet-hedging strategies to cope with rapidly changing environments. One example is non-growing cells in clonal bacterial populations that are able to persist antibiotic treatment. Previous studies suggest that persisters arise in bacterial populations either stochastically through variation in levels of global signalling molecules between individual cells, or in response to various stresses. Here, we show that toxins used in contact-dependent growth inhibition (CDI) create persisters upon direct contact with cells lacking sufficient levels of CdiI immunity protein, which would otherwise bind to and neutralize toxin activity. CDI-mediated persisters form through a feedforward cycle where the toxic activity of the CdiA toxin increases cellular (p)ppGpp levels, which results in Lon-mediated degradation of the immunity protein and more free toxin. Thus, CDI systems mediate a population density-dependent bet-hedging strategy, where the fraction of non-growing cells is increased only when there are many cells of the same genotype. This may be one of the mechanisms of how CDI systems increase the fitness of their hosts.

Indexed as

Cytosine NucleotidesDrug Resistance, BacterialEscherichia coliEscherichia coli ProteinsGenotypeMembrane ProteinsCdiA protein, E colicytidine 3'-diphosphate 5'-diphosphateCytosine NucleotidesEscherichia coli ProteinsMembrane Proteinsbet‐hedgingcontact‐dependent growth inhibitionpersisterstoxin

Identifiers

PMID29572241
PMCPMC5920241

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.