Evidence map›Paper›PMID 28826839›Full record

ArticleCell host & microbe2017

Broad Targeting Specificity during Bacterial Type III CRISPR-Cas Immunity Constrains Viral Escape.

Nora C Pyenson, Kaitlyn Gayvert, Andrew Varble, Olivier Elemento, Luciano A Marraffini

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

82 citing papers in PubMed, 144 citations in OpenAlex.

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  13. Genetic Engineering of Therapeutic Phages Using Type III CRISPR-Cas Systems.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
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22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Nora C PyensonLaboratory of Bacteriology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Kaitlyn GayvertHRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine, Department of Physiology and Biophysics, Weill Cornell Medical College, Cornell University, New York, NY 10021, USA; Tri-Institutional Graduate Program on Computational Biology and Medicine, New York, NY 10065, USA.
Andrew VarbleLaboratory of Bacteriology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Olivier ElementoHRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine, Department of Physiology and Biophysics, Weill Cornell Medical College, Cornell University, New York, NY 10021, USA.
Luciano A MarraffiniLaboratory of Bacteriology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA. Electronic address: marraffini@rockefeller.edu.
Rockefeller University · USCornell University · US

Funding

Tri-Institutional Training Program in Computational Biology & MedicineT32GM083937 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHRISTINI, DAVID J. · 2009 to 2018
$3.1M
The identification and validation of mechanisms and biomarkers for relapse in diffuse large B-cell lymphoma (Administrative Supplement)R01CA194547 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI ELEMENTO, OLIVIER, TAM, WAYNE · 2015 to 2019
$2.6M
Using CRISPR immunity to prevent the spread of virulence traits among pathogensDP2AI104556 · NIAID · ROCKEFELLER UNIVERSITY · PI MARRAFFINI, LUCIANO A · 2012 to 2012
$2.5M
The joint WCM-NYGC Center for Functional and Clinical Interpretation of Tumor ProfilesU24CA210989 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI ELEMENTO, OLIVIER, ZODY, MICHAEL C · 2016 to 2020
$2.4M
NCI NIH HHS R01 CA194547NCI NIH HHS U24 CA210989NIAID NIH HHS DP2 AI104556NIGMS NIH HHS T32 GM083937
6 · The paper itself

Abstract

CRISPR loci are a cluster of repeats separated by short "spacer" sequences derived from prokaryotic viruses and plasmids that determine the targets of the host's CRISPR-Cas immune response against its invaders. For type I and II CRISPR-Cas systems, single-nucleotide mutations in the seed or protospacer adjacent motif (PAM) of the target sequence cause immune failure and allow viral escape. This is overcome by the acquisition of multiple spacers that target the same invader. Here we show that targeting by the Staphylococcus epidermidis type III-A CRISPR-Cas system does not require PAM or seed sequences, and thus prevents viral escape via single-nucleotide substitutions. Instead, viral escapers can only arise through complete target deletion. Our work shows that, as opposed to type I and II systems, the relaxed specificity of type III CRISPR-Cas targeting provides robust immune responses that can lead to viral extinction with a single spacer targeting an essential phage sequence.

Indexed as

CRISPR-Cas SystemsBacterial ProteinsBacteriophagesHost-Pathogen InteractionsStaphylococcus epidermidisBacterial Proteinsadaptive immunitybacteriabacteriophageCasCRISPRCsmplasmid conjugationstaphylococcus

Identifiers

PMID28826839
PMCPMC5599366
OpenAlexW2746479077

What OpenQuestion holds

Textmetadata
LicenceTDM
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.