Evidence map›Paper›PMID 29302058›Full record

ArticleNature communications2018

Incomplete prophage tolerance by type III-A CRISPR-Cas systems reduces the fitness of lysogenic hosts.

Gregory W Goldberg, Elizabeth A McMillan, Andrew Varble, Joshua W Modell, Poulami Samai, Wenyan Jiang, Luciano A Marraffini

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Engineered transcription-associated Cas9 targeting in eukaryotic cells.bioRxiv : the preprint server for biology · 2024
    Article
  6. Applied and environmental microbiology · 2024
    Article
  7. Article
  8. CRISPR-Cas Controls Cryptic Prophages.International journal of molecular sciences · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. RNA-Targeting CRISPR-Cas Systems and Their Applications.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Review
  19. The effect of bacterial mutation rate on the evolution of CRISPR-Cas adaptive immunity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    Article
  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

7 authors at 1 institution in 1 country.

Gregory W GoldbergLaboratory of Bacteriology, The Rockefeller University, New York, NY, 10065, USA.
Elizabeth A McMillanLaboratory of Systems Cancer Biology, The Rockefeller University, New York, NY, 10065, USA.
Andrew VarbleLaboratory of Bacteriology, The Rockefeller University, New York, NY, 10065, USA.
Joshua W ModellLaboratory of Bacteriology, The Rockefeller University, New York, NY, 10065, USA.
Poulami SamaiLaboratory of Bacteriology, The Rockefeller University, New York, NY, 10065, USA.
Wenyan JiangLaboratory of Bacteriology, The Rockefeller University, New York, NY, 10065, USA.
Luciano A MarraffiniLaboratory of Bacteriology, The Rockefeller University, New York, NY, 10065, USA. marraffini@rockefeller.edu.
Rockefeller University · US

Funding

Generation of immunological memory by CRISPR-Cas systemsDP1GM128184 · NIGMS · ROCKEFELLER UNIVERSITY · PI MARRAFFINI, LUCIANO A · 2017 to 2021
$5.9M
Immunity and Infectious DiseaseT32AI070084 · NIAID · ROCKEFELLER UNIVERSITY · PI Michel C Nussenzweig · 2008 to 2026
$3.3M
NIAID NIH HHS T32 AI070084NIGMS NIH HHS DP1 GM128184Wellcome Trust
6 · The paper itself

Abstract

CRISPR-Cas systems offer an immune mechanism through which prokaryotic hosts can acquire heritable resistance to genetic parasites, including temperate phages. Co-transcriptional DNA and RNA targeting by type III-A CRISPR-Cas systems restricts temperate phage lytic infections while allowing lysogenic infections to be tolerated under conditions where the prophage targets are transcriptionally repressed. However, long-term consequences of this phenomenon have not been explored. Here we show that maintenance of conditionally tolerant type III-A systems can produce fitness costs within populations of Staphylococcus aureus lysogens. The fitness costs depend on the activity of prophage-internal promoters and type III-A Cas nucleases implicated in targeting, can be more severe in double lysogens, and are alleviated by spacer-target mismatches which do not abrogate immunity during the lytic cycle. These findings suggest that persistence of type III-A systems that target endogenous prophages could be enhanced by spacer-target mismatches, particularly among populations that are prone to polylysogenization.

Indexed as

BacteriophagesProphagesCRISPR-Cas SystemsLysogenyStaphylococcus aureusStaphylococcus epidermidisVirus Diseases

Identifiers

PMID29302058
PMCPMC5754349
OpenAlexW2780359324

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.