Evidence map›Paper›PMID 31506266›Full record

ArticlemSystems2019

Bioinformatics Identification of Anti-CRISPR Loci by Using Homology, Guilt-by-Association, and CRISPR Self-Targeting Spacer Approaches.

Yanbin Yin, Bowen Yang, Sarah Entwistle

Open access · goldAbstract read
In one paragraph

Article in mSystems, 2019. 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
2.8field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. AcrDB update: Predicted 3D structures of anti-CRISPRs in human gut viromes.Protein science : a publication of the Protein Society · 2025
    Article
  3. Article
  4. Review
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  16. Article
  17. Article
  18. Digging into the lesser-known aspects of CRISPR biology.International microbiology : the official journal of the Spanish Society for Microbiology · 2021
    Review
  19. Crystal structure of the anti-CRISPR repressor Aca2.Journal of structural biology · 2021
    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

3 authors at 2 institutions in 1 country.

Yanbin YinNebraska Food for Health Center, Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, Nebraska, USA yyin@unl.edu.ORCID https://orcid.org/0000-0001-7667-881X
Bowen YangNebraska Food for Health Center, Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
Sarah EntwistleDepartment of Biological Sciences, Northern Illinois University, DeKalb, Illinois, USA.
University of Nebraska–Lincoln · USNorthern Illinois University · US

Funding

Orphan genes in pathogenic bacteriaR15GM114706 · NIGMS · NORTHERN ILLINOIS UNIVERSITY · PI YIN, YANBIN · 2015 to 2015
$373k
NIGMS NIH HHS R15 GM114706
6 · The paper itself

Abstract

Anti-CRISPR (Acr) loci/operons encode Acr proteins and Acr-associated (Aca) proteins. Forty-five Acr families have been experimentally characterized inhibiting seven subtypes of CRISPR-Cas systems. We have developed a bioinformatics pipeline to identify genomic loci containing Acr homologs and/or Aca homologs by combining three computational approaches: homology, guilt-by-association, and self-targeting spacers. Homology search found thousands of Acr homologs in bacterial and viral genomes, but most are homologous to AcrIIA7 and AcrIIA9. Investigating the gene neighborhood of these Acr homologs revealed that only a small percentage (23.0% in bacteria and 8.2% in viruses) of them have neighboring Aca homologs and thus form Acr-Aca operons. Surprisingly, although a self-targeting spacer is a strong indicator of the presence of Acr genes in a genome, a large percentage of Acr-Aca loci are found in bacterial genomes without self-targeting spacers or even without complete CRISPR-Cas systems. Additionally, for Acr homologs from genomes with self-targeting spacers, homology-based Acr family assignments do not always agree with the self-targeting CRISPR-Cas subtypes. Last, by investigating Acr genomic loci coexisting with self-targeting spacers in the same genomes, five known subtypes (I-C, I-E, I-F, II-A, and II-C) and five new subtypes (I-B, III-A, III-B, IV-A, and V-U4) of Acrs were inferred. Based on these findings, we conclude that the discovery of new anti-CRISPRs should not be restricted to genomes with self-targeting spacers and loci with Acr homologs. The evolutionary arms race of CRISPR-Cas systems and anti-CRISPR systems may have driven the adaptive and rapid gain and loss of these elements in closely related genomes.

Indexed as

AcaAcranti-CRISPRCRISPR-CasCRISPR self-targetinggene neighborhoodgenomic islandhelix-turn-helixphageprophage

Identifiers

PMID31506266
PMCPMC6739104
OpenAlexW2973025767

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.