Evidence map›Paper›PMID 38427560›Full record

ArticleCell reports2024

Anti-CRISPR proteins trigger a burst of CRISPR-Cas9 expression that enhances phage defense.

Rachael E Workman, Marie J Stoltzfus, Nicholas C Keith, Chad W Euler, Joseph Bondy-Denomy, Joshua W Modell

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.1field-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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
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  7. Bacteriophage Therapy AgainstMicroorganisms · 2026
    Review
  8. Review
  9. Article
  10. Viral effectors trigger innate immunity across the tree of life.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  11. Article
  12. Article
  13. Article
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  15. Article
  16. Review
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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

6 authors at 3 institutions in 1 country.

Rachael E WorkmanDepartment of Molecular Biology & Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Marie J StoltzfusDepartment of Molecular Biology & Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Nicholas C KeithDepartment of Molecular Biology & Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Chad W EulerDepartment of Medical Laboratory Sciences, Hunter College, CUNY, New York, NY 10021, USA; Department of Microbiology and Immunology, Weill Cornell Medical College, New York, NY 10021, USA.
Joseph Bondy-DenomyDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94158, USA; Quantitative Biosciences Institute, University of California, San Francisco, San Francisco, CA 94158, USA; Innovative Genomics Institute, Berkeley, CA, USA.
Joshua W ModellDepartment of Molecular Biology & Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address: jmodell1@jhmi.edu.
Johns Hopkins University · USCornell University · USQB3 · US

Funding

Non-canonical functions of Cas9 andthe cell biology of CRISPR-Cas immunityR35GM142731 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI Joshua Modell · 2021 to 2026
$2.6M
NIGMS NIH HHS R35 GM142731
6 · The paper itself

Abstract

CRISPR-Cas immune systems provide bacteria with adaptive immunity against bacteriophages, but they are often transcriptionally repressed to mitigate auto-immunity. In some cases, CRISPR-Cas expression increases in response to a phage infection, but the mechanisms of induction are largely unknown, and it is unclear whether induction occurs strongly and quickly enough to benefit the bacterial host. In S. pyogenes, Cas9 is both an immune effector and auto-repressor of CRISPR-Cas expression. Here, we show that phage-encoded anti-CRISPR proteins relieve Cas9 auto-repression and trigger a rapid increase in CRISPR-Cas levels during a single phage infective cycle. As a result, fewer cells succumb to lysis, leading to a striking survival benefit after multiple rounds of infection. CRISPR-Cas induction also reduces lysogeny, thereby limiting a route for horizontal gene transfer. Altogether, we show that Cas9 is not only a CRISPR-Cas effector and repressor but also a phage sensor that can mount an anti-anti-CRISPR transcriptional response.

Indexed as

BacteriophagesBacteriaCRISPR-Cas SystemsLysogenyViral ProteinsViral Proteinsanti-CRISPRbacterial immunitybacteriophageCP: MicrobiologyCRISPR

Identifiers

PMID38427560
PMCPMC11078563
OpenAlexW4392528814

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.