Evidence map›Paper›PMID 34172748›Full record

ArticleNature communications2021

A genetically encoded anti-CRISPR protein constrains gene drive spread and prevents population suppression.

Chrysanthi Taxiarchi, Andrea Beaghton, Nayomi Illansinhage Don, Kyros Kyrou, Matthew Gribble, Dammy Shittu, Scott P Collins, Chase L Beisel, Roberto Galizi, Andrea Crisanti

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 56 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

10 authors at 4 institutions in 4 countries.

Chrysanthi TaxiarchiDepartment of Life Sciences, Imperial College London, London, UK.ORCID 0000-0002-6616-5241
Andrea BeaghtonDepartment of Life Sciences, Imperial College London, London, UK.
Nayomi Illansinhage DonDepartment of Life Sciences, Imperial College London, London, UK.
Kyros KyrouDepartment of Life Sciences, Imperial College London, London, UK.ORCID 0000-0002-4919-2459
Matthew GribbleDepartment of Life Sciences, Imperial College London, London, UK.
Dammy ShittuDepartment of Life Sciences, Imperial College London, London, UK.
Scott P CollinsDepartment of Chemical and Biomolecular Engineering, North Carolina State University, Raleigh, NC, USA.
Chase L BeiselDepartment of Chemical and Biomolecular Engineering, North Carolina State University, Raleigh, NC, USA.ORCID 0000-0003-0650-9943
Roberto GaliziCentre for Applied Entomology and Parasitology, School of Life Sciences, Keele University, Keele, UK. r.galizi@outlook.com.ORCID 0000-0003-3134-7480
Andrea CrisantiDepartment of Life Sciences, Imperial College London, London, UK. acrs@imperial.ac.uk.
Imperial College London · GBNorth Carolina State University · USKeele University · GBUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CRISPR-based gene drives offer promising means to reduce the burden of pests and vector-borne diseases. These techniques consist of releasing genetically modified organisms carrying CRISPR-Cas nucleases designed to bias their inheritance and rapidly propagate desired modifications. Gene drives can be intended to reduce reproductive capacity of harmful insects or spread anti-pathogen effectors through wild populations, even when these confer fitness disadvantages. Technologies capable of halting the spread of gene drives may prove highly valuable in controlling, counteracting, and even reverting their effect on individual organisms as well as entire populations. Here we show engineering and testing of a genetic approach, based on the germline expression of a phage-derived anti-CRISPR protein (AcrIIA4), able to inactivate CRISPR-based gene drives and restore their inheritance to Mendelian rates in the malaria vector Anopheles gambiae. Modeling predictions and cage testing show that a single release of male mosquitoes carrying the AcrIIA4 protein can block the spread of a highly effective suppressive gene drive preventing population collapse of caged malaria mosquitoes.

Indexed as

AnimalsAnimals, Genetically ModifiedAnophelesBacterial ProteinsCRISPR-Associated Protein 9CRISPR-Cas SystemsFemaleFertilityGene Drive TechnologyGenetic FitnessGenetics, PopulationListeria monocytogenesMaleBacterial ProteinsCRISPR-Associated Protein 9

Identifiers

PMID34172748
PMCPMC8233359
OpenAlexW3176880777

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.