Evidence map›Paper›PMID 32053108›Full record

ArticleeLife2020

A large-scale resource for tissue-specific CRISPR mutagenesis in

Fillip Port, Claudia Strein, Mona Stricker, Benedikt Rauscher, Florian Heigwer, Jun Zhou, Celine Beyersdörffer, Jana Frei, Amy Hess, Katharina Kern and 9 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
10.3field-weighted citation impact, top 1% 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

98 citing papers in PubMed, 175 citations in OpenAlex.

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  10. Disruption of a selective vesicle pool upon retrograde amnesia dissociates memory at presynaptic terminals.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  13. Frontiers in cellular and infection microbiology · 2026
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38 more citing papers are in PubMed but not listed here.

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

19 authors at 1 institution in 1 country.

Fillip PortGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.ORCID 0000-0002-5157-4835
Claudia StreinGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Mona StrickerGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Benedikt RauscherGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Florian HeigwerGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.ORCID 0000-0002-8230-1485
Jun ZhouGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.ORCID 0000-0002-2101-9304
Celine BeyersdörfferGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Jana FreiGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Amy HessGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Katharina KernGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Laura LangeGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Nora LangnerGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Roberta MalamudGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Bojana PavlovićGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Kristin RädeckeGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Lukas SchmittGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Lukas VoosGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Erica ValentiniGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.
Michael BoutrosGerman Cancer Research Center (DKFZ), Division Signaling and Functional Genomics and Heidelberg University, Heidelberg, Germany.ORCID 0000-0002-9458-817X
German Cancer Research Center · DE

Funding

Deutsche Forschungsgemeinschaft SFB1324Deutsche Forschungsgemeinschaft SFB/TRR186Deutsche Forschungsgemeinschaft TRR186European Research Council DecodeEuropean Research Council DECODE
6 · The paper itself

Abstract

Genetic screens are powerful tools for the functional annotation of genomes. In the context of multicellular organisms, interrogation of gene function is greatly facilitated by methods that allow spatial and temporal control of gene abrogation. Here, we describe a large-scale transgenic short guide (sg) RNA library for efficient CRISPR-based disruption of specific target genes in a constitutive or conditional manner. The library consists currently of more than 2600 plasmids and 1700 fly lines with a focus on targeting kinases, phosphatases and transcription factors, each expressing two sgRNAs under control of the Gal4/UAS system. We show that conditional CRISPR mutagenesis is robust across many target genes and can be efficiently employed in various somatic tissues, as well as the germline. In order to prevent artefacts commonly associated with excessive amounts of Cas9 protein, we have developed a series of novel UAS-Cas9 transgenes, which allow fine tuning of Cas9 expression to achieve high gene editing activity without detectable toxicity. Functional assays, as well as direct sequencing of genomic sgRNA target sites, indicates that the vast majority of transgenic sgRNA lines mediate efficient gene disruption. Furthermore, we conducted the so far largest fully transgenic CRISPR screen in any metazoan organism, which further supported the high efficiency and accuracy of our library and revealed many so far uncharacterized genes essential for development.

Indexed as

CRISPR-Associated Protein 9CRISPR-Cas SystemsAnimalsAnimals, Genetically ModifiedDrosophila melanogasterGene EditingRNACRISPR-Associated Protein 9RNAconditional mutagenesisCRISPRdevelopmental biologyD. melanogastergeneticsgenetic toolsgenomicslarge-scale in vivo screensResource

Identifiers

PMID32053108
PMCPMC7062466
OpenAlexW3005664759

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.