Evidence map›Paper›PMID 19543290›Full record

ArticleNature structural & molecular biology2009

Control of alternative splicing through siRNA-mediated transcriptional gene silencing.

Mariano Alló, Valeria Buggiano, Juan P Fededa, Ezequiel Petrillo, Ignacio Schor, Manuel de la Mata, Eneritz Agirre, Mireya Plass, Eduardo Eyras, Sherif Abou Elela and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature structural & molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 210 papers.

0numbers the graph read from it
0cells of the map it votes in
210citing papers in PubMed
11.8field-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

210 citing papers in PubMed, 336 citations in OpenAlex.

  1. RNA splicing in health and disease.Molecular biomedicine · 2026
    Review
  2. Article
  3. Article
  4. RNA-binding proteins connect Exon usage to the chromatin.NAR genomics and bioinformatics · 2025
    Article
  5. Review
  6. Article
  7. Alternative Splicing Regulation in Metabolic Disorders.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
    Review
  8. Nuclear Roles of Spliceosome-Associated microRNAs in Neuronal Cancer Cells.International journal of molecular sciences · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

150 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

13 authors at 6 institutions in 3 countries.

Mariano AllóLaboratorio de Fisiología y Biología Molecular, Departamento de Fisiología, Biología Molecular y Celular, IFIBYNE-CONICET, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Buenos Aires, Argentina.
Valeria Buggiano
Juan P Fededa
Ezequiel Petrillo
Ignacio Schor
Manuel de la Mata
Eneritz Agirre
Mireya Plass
Eduardo Eyras
Sherif Abou Elela
Roscoe Klinck
Benoit Chabot
Alberto R Kornblihtt
Consejo Nacional de Investigaciones Científicas y Técnicas · ARUniversité de Sherbrooke · CAFundación Ciencias Exactas y Naturales · ARPompeu Fabra University · ESInstitució Catalana de Recerca i Estudis Avançats · ESUniversity of Buenos Aires · AR

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

When targeting promoter regions, small interfering RNAs (siRNAs) trigger a previously proposed pathway known as transcriptional gene silencing by promoting heterochromatin formation. Here we show that siRNAs targeting intronic or exonic sequences close to an alternative exon regulate the splicing of that exon. The effect occurred in hepatoma and HeLa cells with siRNA antisense strands designed to enter the silencing pathway, suggesting hybridization with nascent pre-mRNA. Unexpectedly, in HeLa cells the sense strands were also effective, suggesting that an endogenous antisense transcript, detectable in HeLa but not in hepatoma cells, acts as a target. The effect depends on Argonaute-1 and is counterbalanced by factors favoring chromatin opening or transcriptional elongation. The increase in heterochromatin marks (dimethylation at Lys9 and trimethylation at Lys27 of histone H3) at the target site, the need for the heterochromatin-associated protein HP1alpha and the reduction in RNA polymerase II processivity suggest a mechanism involving the kinetic coupling of transcription and alternative splicing.

Indexed as

Alternative SplicingRNA InterferenceRNA, Small InterferingTranscription, GeneticAnimalsArgonaute ProteinsBase SequenceCarcinoma, HepatocellularChromobox Protein Homolog 5Epigenesis, GeneticEukaryotic Initiation FactorsExonsFibronectinsGene Knockdown TechniquesHeLa CellsHeterochromatinAGO1 protein, humanArgonaute ProteinsCBX5 protein, humanChromobox Protein Homolog 5Eukaryotic Initiation FactorsFibronectinsHeterochromatinHistonesLysineOligonucleotides, AntisenseRibonuclease IIIRNA Polymerase IIRNA, Small Interfering

Identifiers

PMID19543290
OpenAlexW1992332038

What OpenQuestion holds

Textmetadata
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.