Evidence map›Paper›PMID 33406240›Full record

ArticleNucleic acids research2021

Targeting alternative splicing by RNAi: from the differential impact on splice variants to triggering artificial pre-mRNA splicing.

Armin Fuchs, Stefan Riegler, Zahra Ayatollahi, Nicola Cavallari, Luciana E Giono, Barbara A Nimeth, Krishna V Mutanwad, Alois Schweighofer, Doris Lucyshyn, Andrea Barta and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

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  11. Lipid-based nucleic acid therapeutics with in vivo efficacy.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2023
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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 4 institutions in 2 countries.

Armin FuchsMax Perutz Labs, Medical University of Vienna, Vienna 1030, Austria.
Stefan RieglerMax Perutz Labs, Medical University of Vienna, Vienna 1030, Austria.
Zahra AyatollahiMax Perutz Labs, Medical University of Vienna, Vienna 1030, Austria.
Nicola CavallariMax Perutz Labs, Medical University of Vienna, Vienna 1030, Austria.
Luciana E GionoInstituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE), CONICET-Universidad de Buenos Aires, C1428EHA, Buenos Aires, Argentina.
Barbara A NimethDepartment of Applied Genetics and Cell Biology, University of Natural Resources and Life Sciences Vienna, Vienna 1190, Austria.
Krishna V MutanwadDepartment of Applied Genetics and Cell Biology, University of Natural Resources and Life Sciences Vienna, Vienna 1190, Austria.
Alois SchweighoferMax Perutz Labs, University of Vienna, Vienna 1030, Austria.
Doris LucyshynDepartment of Applied Genetics and Cell Biology, University of Natural Resources and Life Sciences Vienna, Vienna 1190, Austria.
Andrea BartaMax Perutz Labs, Medical University of Vienna, Vienna 1030, Austria.
Ezequiel PetrilloMax Perutz Labs, Medical University of Vienna, Vienna 1030, Austria.
Maria KalynaDepartment of Applied Genetics and Cell Biology, University of Natural Resources and Life Sciences Vienna, Vienna 1190, Austria.
Max Perutz Labs · ATBOKU University · ATConsejo Nacional de Investigaciones Científicas y Técnicas · ARUniversity of Vienna · AT

Funding

Austrian Science Fund FWF P 26333
6 · The paper itself

Abstract

Alternative splicing generates multiple transcript and protein isoforms from a single gene and controls transcript intracellular localization and stability by coupling to mRNA export and nonsense-mediated mRNA decay (NMD). RNA interference (RNAi) is a potent mechanism to modulate gene expression. However, its interactions with alternative splicing are poorly understood. We used artificial microRNAs (amiRNAs, also termed shRNAmiR) to knockdown all splice variants of selected target genes in Arabidopsis thaliana. We found that splice variants, which vary by their protein-coding capacity, subcellular localization and sensitivity to NMD, are affected differentially by an amiRNA, although all of them contain the target site. Particular transcript isoforms escape amiRNA-mediated degradation due to their nuclear localization. The nuclear and NMD-sensitive isoforms mask RNAi action in alternatively spliced genes. Interestingly, Arabidopsis SPL genes, which undergo alternative splicing and are targets of miR156, are regulated in the same manner. Moreover, similar results were obtained in mammalian cells using siRNAs, indicating cross-kingdom conservation of these interactions among RNAi and splicing isoforms. Furthermore, we report that amiRNA can trigger artificial alternative splicing, thus expanding the RNAi functional repertoire. Our findings unveil novel interactions between different post-transcriptional processes in defining transcript fates and regulating gene expression.

Indexed as

Gene Knockdown TechniquesNonsense Mediated mRNA DecayRNA InterferenceAlternative SplicingArabidopsisArabidopsis ProteinsExonsGene Expression Regulation, PlantGenes, PlantHeLa CellsHumansMicroRNAsPlants, Genetically ModifiedProtein IsoformsProtoplastsRNA, PlantArabidopsis ProteinsMicroRNAsProtein IsoformsRNA, PlantRNA PrecursorsSerine-Arginine Splicing FactorsSRSF4 protein, human

Identifiers

PMID33406240
PMCPMC7826280
OpenAlexW3119334400

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.