Evidence map›Paper›PMID 27280787›Full record

ArticleG3 (Bethesda, Md.)2016

A Combination of CRISPR/Cas9 and Standardized RNAi as a Versatile Platform for the Characterization of Gene Function.

Sebastian Wissel, Anja Kieser, Tetsuo Yasugi, Peter Duchek, Elisabeth Roitinger, Joseph Gokcezade, Victoria Steinmann, Ulrike Gaul, Karl Mechtler, Klaus Förstemann and 2 more

Open access · goldAbstract read
In one paragraph

Article in G3 (Bethesda, Md.), 2016. 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
2.6field-weighted citation impact, top 10% 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, 22 citations in OpenAlex.

  1. Article
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  3. Cells · 2022
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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

12 authors at 2 institutions in 2 countries.

Sebastian WisselInstitute of Molecular Biotechnology Austria, 1030 Vienna, Austria.
Anja KieserGene Center, Ludwig-Maximilians-University Munich, 81377, Germany.
Tetsuo YasugiInstitute of Molecular Biotechnology Austria, 1030 Vienna, Austria.
Peter DuchekInstitute of Molecular Biotechnology Austria, 1030 Vienna, Austria.
Elisabeth RoitingerInstitute of Molecular Biotechnology Austria, 1030 Vienna, Austria Institute of Molecular Pathology, 1030 Vienna, Austria.
Joseph GokcezadeInstitute of Molecular Biotechnology Austria, 1030 Vienna, Austria.
Victoria SteinmannInstitute of Molecular Biotechnology Austria, 1030 Vienna, Austria.
Ulrike GaulGene Center, Ludwig-Maximilians-University Munich, 81377, Germany.
Karl MechtlerInstitute of Molecular Biotechnology Austria, 1030 Vienna, Austria Institute of Molecular Pathology, 1030 Vienna, Austria.
Klaus FörstemannGene Center, Ludwig-Maximilians-University Munich, 81377, Germany.
Jürgen A KnoblichInstitute of Molecular Biotechnology Austria, 1030 Vienna, Austria juergen.knoblich@imba.oeaw.ac.at ralph.neumueller@boehringer-ingelheim.com.ORCID 0000-0002-6751-3404
Ralph A NeumüllerInstitute of Molecular Biotechnology Austria, 1030 Vienna, Austria Gene Center, Ludwig-Maximilians-University Munich, 81377, Germany juergen.knoblich@imba.oeaw.ac.at ralph.neumueller@boehringer-ingelheim.com.
Institute of Molecular Biotechnology · ATLudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traditional loss-of-function studies in Drosophila suffer from a number of shortcomings, including off-target effects in the case of RNA interference (RNAi) or the stochastic nature of mosaic clonal analysis. Here, we describe minimal in vivo GFP interference (miGFPi) as a versatile strategy to characterize gene function and to conduct highly stringent, cell type-specific loss-of-function experiments in Drosophila miGFPi combines CRISPR/Cas9-mediated tagging of genes at their endogenous locus with an immunotag and an exogenous 21 nucleotide RNAi effector sequence with the use of a single reagent, highly validated RNAi line targeting this sequence. We demonstrate the utility and time effectiveness of this method by characterizing the function of the Polymerase I (Pol I)-associated transcription factor Tif-1a, and the previously uncharacterized gene MESR4, in the Drosophila female germline stem cell lineage. In addition, we show that miGFPi serves as a powerful technique to functionally characterize individual isoforms of a gene. We exemplify this aspect of miGFPi by studying isoform-specific loss-of-function phenotypes of the longitudinals lacking (lola) gene in neural stem cells. Altogether, the miGFPi strategy constitutes a generalized loss-of-function approach that is amenable to the study of the function of all genes in the genome in a stringent and highly time effective manner.

Indexed as

CRISPR-Cas SystemsRNA InterferenceAnimalsAnimals, Genetically ModifiedCell NucleusDrosophilaDrosophila ProteinsFemaleGerm CellsGreen Fluorescent ProteinsMutationProtein IsoformsRepressor ProteinsRNA, Guide, CRISPR-Cas SystemsStem CellsTranscription FactorsDrosophila ProteinsGreen Fluorescent ProteinsMESR4 protein, DrosophilaProtein IsoformsRepressor ProteinsRNA, Guide, CRISPR-Cas SystemsTif-IA protein, DrosophilaTranscription FactorsCRISPRDrosophilaloss-of-functionstem cell

Identifiers

PMID27280787
PMCPMC4978900
OpenAlexW2409531854

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.