Evidence map›Paper›PMID 34154416›Full record

ArticlemBio2021

Bacteriophage T4 Escapes CRISPR Attack by Minihomology Recombination and Repair.

Xiaorong Wu, Jingen Zhu, Pan Tao, Venigalla B Rao

Open access · goldAbstract read
In one paragraph

Article in mBio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Bacteriophage genome-wide transposon mutagenesis.bioRxiv : the preprint server for biology · 2025
    Article
  4. Rapid detection ofActa biochimica et biophysica Sinica · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. CRISPR-Cas12a exhibits metal-dependent specificity switching.bioRxiv : the preprint server for biology · 2024
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
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  20. Review
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.

Xiaorong WuBacteriophage Medical Research Center, Department of Biology, The Catholic University of America, Washington, DC, USA.
Jingen ZhuBacteriophage Medical Research Center, Department of Biology, The Catholic University of America, Washington, DC, USA.
Pan TaoBacteriophage Medical Research Center, Department of Biology, The Catholic University of America, Washington, DC, USA.
Venigalla B RaoBacteriophage Medical Research Center, Department of Biology, The Catholic University of America, Washington, DC, USA.
University of America · US

Funding

Structural studies of bacteriophage T4 and their potential medical applicationsR01AI081726 · NIAID · PURDUE UNIVERSITY · PI KUHN, RICHARD J., RAO, VENIGALLA B. · 2010 to 2019
$6.2M
Structural studies of bacteriophage T4 and their potential medical applicationsR56AI081726 · NIAID · PURDUE UNIVERSITY · PI ROSSMANN, MICHAEL G · 2009 to 2009
$600k
NIAID NIH HHS R01 AI081726NIAID NIH HHS R56 AI081726
6 · The paper itself

Abstract

Bacteria and bacteriophages (phages) have evolved potent defense and counterdefense mechanisms that allowed their survival and greatest abundance on Earth. CRISPR (clustered regularly interspaced short palindromic repeat)-Cas (CRISPR-associated) is a bacterial defense system that inactivates the invading phage genome by introducing double-strand breaks at targeted sequences. While the mechanisms of CRISPR defense have been extensively investigated, the counterdefense mechanisms employed by phages are poorly understood. Here, we report a novel counterdefense mechanism by which phage T4 restores the genomes broken by CRISPR cleavages. Catalyzed by the phage-encoded recombinase UvsX, this mechanism pairs very short stretches of sequence identity (minihomology sites), as few as 3 or 4 nucleotides in the flanking regions of the cleaved site, allowing replication, repair, and stitching of genomic fragments. Consequently, a series of deletions are created at the targeted site, making the progeny genomes completely resistant to CRISPR attack. Our results demonstrate that this is a general mechanism operating against both type II (Cas9) and type V (Cas12a) CRISPR-Cas systems. These studies uncovered a new type of counterdefense mechanism evolved by T4 phage where subtle functional tuning of preexisting DNA metabolism leads to profound impact on phage survival.

Indexed as

DNA RepairRecombination, GeneticBacteriophage T4CRISPR-Cas SystemsGenome, Viralbacteriophage T4CRISPR-Cas genome editingend joininghomologous recombinationphage counterdefenseUvsX recombinase

Identifiers

PMID34154416
PMCPMC8262927
OpenAlexW3173173390

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.