Evidence map›Paper›PMID 25246539›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Precisely modulated pathogenicity island interference with late phage gene transcription.

Geeta Ram, John Chen, Hope F Ross, Richard P Novick

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.6field-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

42 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Capsid redirection mechanism of thePhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Article
  3. Genetics, ecology and evolution of phage satellites.Nature reviews. Microbiology · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Atopic dermatitis-derivedFrontiers in cellular and infection microbiology · 2023
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
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  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

4 authors at 2 institutions in 1 country.

Geeta RamSkirball Institute Program in Molecular Pathogenesis and Departments of Microbiology and Medicine, New York University Medical Center, New York, NY 10016.
John ChenSkirball Institute Program in Molecular Pathogenesis and Departments of Microbiology and Medicine, New York University Medical Center, New York, NY 10016.
Hope F RossSkirball Institute Program in Molecular Pathogenesis and Departments of Microbiology and Medicine, New York University Medical Center, New York, NY 10016.
Richard P NovickSkirball Institute Program in Molecular Pathogenesis and Departments of Microbiology and Medicine, New York University Medical Center, New York, NY 10016 richard.novick@med.nyu.edu.
New York University · USUniversity Medical Center · US

Funding

Molecular Biology of TSST-1 and other superantigen toxinsR01AI022159 · NIAID · PUBLIC HEALTH RESEARCH INSTITUTE · PI NOVICK, RICHARD P. · 1985 to 2014
$2.6M
NIAID NIH HHS R01 AI022159NIAID NIH HHS R01AI022159
6 · The paper itself

Abstract

Having gone to great evolutionary lengths to develop resistance to bacteriophages, bacteria have come up with resistance mechanisms directed at every aspect of the bacteriophage life cycle. Most genes involved in phage resistance are carried by plasmids and other mobile genetic elements, including bacteriophages and their relatives. A very special case of phage resistance is exhibited by the highly mobile phage satellites, staphylococcal pathogenicity islands (SaPIs), which carry and disseminate superantigen and other virulence genes. Unlike the usual phage-resistance mechanisms, the SaPI-encoded interference mechanisms are carefully crafted to ensure that a phage-infected, SaPI-containing cell will lyse, releasing the requisite crop of SaPI particles as well as a greatly diminished crop of phage particles. Previously described SaPI interference genes target phage functions that are not required for SaPI particle production and release. Here we describe a SaPI-mediated interference system that affects expression of late phage gene transcription and consequently is required for SaPI and phage. Although when cloned separately, a single SaPI gene totally blocks phage production, its activity in situ is modulated accurately by a second gene, achieving the required level of interference. The advantage for the host bacteria is that the SaPIs curb excessive phage growth while enhancing their gene transfer activity. This activity is in contrast to that of the clustered regularly interspaced short palindromic repeats (CRISPRs), which totally block phage growth at the cost of phage-mediated gene transfer. In staphylococci the SaPI strategy seems to have prevailed during evolution: The great majority of Staphylococcus aureus strains carry one or more SaPIs, whereas CRISPRs are extremely rare.

Indexed as

Transcription, GeneticAmino Acid SequenceBacterial ProteinsBacteriolysisGenomic IslandsHost-Pathogen InteractionsMolecular Sequence DataMutationPlasmidsSequence Homology, Amino AcidStaphylococcus aureusStaphylococcus PhagesSuperantigensViral Plaque AssayViral ProteinsVirulenceBacterial ProteinsSuperantigensViral Proteinsbacteriophage resistancehelper phagetranscription regulation

Identifiers

PMID25246539
PMCPMC4209980
OpenAlexW2089698276

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.