Evidence map›Paper›PMID 24187086›Full record

ArticleJournal of bacteriology2014

Genetic characterization of antiplasmid immunity through a type III-A CRISPR-Cas system.

Asma Hatoum-Aslan, Inbal Maniv, Poulami Samai, Luciano A Marraffini

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bacteriology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

94 citing papers in PubMed, 166 citations in OpenAlex.

  1. Article
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  6. Comparative genomic analysis ofMicrobiology (Reading, England) · 2025
    Article
  7. Article
  8. CRISPR-Cas Systems: A Functional Perspective and Innovations.International journal of molecular sciences · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Genetic Engineering of Therapeutic Phages Using Type III CRISPR-Cas Systems.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Structures of an active type III-A CRISPR effector complex.Structure (London, England : 1993) · 2022
    Article
  20. Article

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

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 1 institution in 1 country.

Asma Hatoum-AslanLaboratory of Bacteriology, The Rockefeller University, New York, New York, USA.
Inbal Maniv
Poulami Samai
Luciano A Marraffini
Rockefeller University · US

Funding

Using CRISPR immunity to prevent the spread of virulence traits among pathogensDP2AI104556 · NIAID · ROCKEFELLER UNIVERSITY · PI MARRAFFINI, LUCIANO A · 2012 to 2012
$2.5M
NIAID NIH HHS 1DP2AI104556-01NIAID NIH HHS DP2 AI104556
6 · The paper itself

Abstract

Many prokaryotes possess an adaptive immune system encoded by clustered regularly interspaced short palindromic repeats (CRISPRs). CRISPR loci produce small guide RNAs (crRNAs) that, in conjunction with flanking CRISPR-associated (cas) genes, combat viruses and block plasmid transfer by an antisense targeting mechanism. CRISPR-Cas systems have been classified into three types (I to III) that employ distinct mechanisms of crRNA biogenesis and targeting. The type III-A system in Staphylococcus epidermidis RP62a blocks the transfer of staphylococcal conjugative plasmids and harbors nine cas-csm genes. Previous biochemical analysis indicated that Cas10, Csm2, Csm3, Csm4, and Csm5 form a crRNA-containing ribonucleoprotein complex; however, the roles of these genes toward antiplasmid targeting remain unknown. Here, we determined the cas-csm genes that are required for antiplasmid immunity and used genetic and biochemical analyses to investigate the functions of predicted motifs and domains within these genes. We found that many mutations affected immunity by impacting the formation of the Cas10-Csm complex or crRNA biogenesis. Surprisingly, mutations in the predicted nuclease domains of the members of the Cas10-Csm complex had no detectable effect on antiplasmid immunity or crRNA biogenesis. In contrast, the deletion of csm6 and mutations in the cas10 Palm polymerase domain prevented CRISPR immunity without affecting either complex formation or crRNA production, suggesting their involvement in target destruction. By delineating the genetic requirements of this system, our findings further contribute to the mechanistic understanding of type III CRISPR-Cas systems.

Indexed as

CRISPR-Cas SystemsGene Transfer, HorizontalPlasmidsDNA Mutational AnalysisGenes, BacterialRibonucleoproteinsRNA, Small InterferingSequence DeletionStaphylococcus epidermidisRibonucleoproteinsRNA, Small Interfering

Identifiers

PMID24187086
PMCPMC3911255
OpenAlexW2032672026

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.