Evidence map›Paper›PMID 35623354›Full record

ArticleMolecular cell2022

Lack of Cas13a inhibition by anti-CRISPR proteins from Leptotrichia prophages.

Matthew C Johnson, Logan T Hille, Benjamin P Kleinstiver, Alexander J Meeske, Joseph Bondy-Denomy

Open access · hybridAbstract read
In one paragraph

Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

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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

5 authors at 4 institutions in 1 country.

Matthew C JohnsonDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94158, USA.
Logan T HillePhD Program in Biological and Biomedical Sciences, Harvard University, Boston, MA 02115, USA; Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA.
Benjamin P KleinstiverCenter for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.
Alexander J MeeskeDepartment of Microbiology, University of Washington, Seattle, WA 98109, USA. Electronic address: meeske@uw.edu.
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 94720, USA. Electronic address: joseph.bondy-denomy@ucsf.edu.
Harvard University · USQB3 · USUniversity of California, San Francisco · USUniversity of Washington · US

Funding

PROJECT 4: Somatic evolution of the hematopoietic system in cardiovascular diseaseP01HL142494 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI Charles P. Lin · 2019 to 2026
$19.5M
CRISPR-Cas13 immunity in Listeria seeligeriR35GM142460 · NIGMS · UNIVERSITY OF WASHINGTON · PI Alexander Jacob Meeske · 2021 to 2026
$2.7M
Discovering New Roles for CRISPR-Cas in Bacterial PathogenesisDP5OD021344 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BONDY-DENOMY, JOSEPH · 2015 to 2019
$2.1M
Uncovering the mechanism and role of a widespread anti-CRISPR-Cas9 proteinR01GM127489 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BONDY-DENOMY, JOSEPH · 2018 to 2022
$1.7M
NHLBI NIH HHS P01 HL142494NIGMS NIH HHS R01 GM127489NIGMS NIH HHS R35 GM142460NIH HHS DP5 OD021344
6 · The paper itself

Abstract

CRISPR systems are prokaryotic adaptive immune systems that use RNA-guided Cas nucleases to recognize and destroy foreign genetic elements. To overcome CRISPR immunity, bacteriophages have evolved diverse families of anti-CRISPR proteins (Acrs). Recently, Lin et al. (2020) described the discovery and characterization of 7 Acr families (AcrVIA1-7) that inhibit type VI-A CRISPR systems. We detail several inconsistencies that question the results reported in the Lin et al. (2020) study. These include inaccurate bioinformatics analyses and bacterial strains that are impossible to construct. Published strains were provided by the authors, but MS2 bacteriophage plaque assays did not support the published results. We also independently tested the Acr sequences described in the original report, in E. coli and mammalian cells, but did not observe anti-Cas13a activity. Taken together, our data and analyses prompt us to question the claim that AcrVIA1-7 reported in Lin et al. are type VI anti-CRISPR proteins.

Indexed as

BacteriophagesCRISPR-Associated ProteinsAnimalsCRISPR-Cas SystemsEscherichia coliLeptotrichiaMammalsProphagesRibonucleasesCRISPR-Associated ProteinsRibonucleasesanti-CRISPRbacteriophagebioinformaticsCas13aprophagereproducibilityRNA-targetingType VI CRISPR-Cas

Identifiers

PMID35623354
PMCPMC9186262
OpenAlexW4281563635

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.