Evidence map›Paper›PMID 33767452›Full record

ArticleNature structural & molecular biology2021

A first exon termination checkpoint preferentially suppresses extragenic transcription.

Liv M I Austenaa, Viviana Piccolo, Marta Russo, Elena Prosperini, Sara Polletti, Danilo Polizzese, Serena Ghisletti, Iros Barozzi, Giuseppe R Diaferia, Gioacchino Natoli

Open access · greenAbstract read
In one paragraph

Article in Nature structural & molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 3 institutions in 2 countries.

Liv M I Austenaa *European Institute of Oncology (IEO) IRCCS, Milan, Italy. livmagnhild.austenaa@ieo.it.
Viviana Piccolo *European Institute of Oncology (IEO) IRCCS, Milan, Italy.
Marta Russo *European Institute of Oncology (IEO) IRCCS, Milan, Italy.
Elena ProsperiniEuropean Institute of Oncology (IEO) IRCCS, Milan, Italy.
Sara PollettiEuropean Institute of Oncology (IEO) IRCCS, Milan, Italy.ORCID http://orcid.org/0000-0002-5433-0502
Danilo PolizzeseEuropean Institute of Oncology (IEO) IRCCS, Milan, Italy.
Serena GhislettiEuropean Institute of Oncology (IEO) IRCCS, Milan, Italy.
Iros BarozziDepartment of Surgery and Cancer, Imperial College London, London, UK.ORCID http://orcid.org/0000-0003-0690-3473
Giuseppe R DiaferiaEuropean Institute of Oncology (IEO) IRCCS, Milan, Italy.ORCID http://orcid.org/0000-0003-4022-8483
Gioacchino NatoliEuropean Institute of Oncology (IEO) IRCCS, Milan, Italy. gioacchino.natoli@ieo.it.ORCID http://orcid.org/0000-0003-0711-2411
Istituti di Ricovero e Cura a Carattere Scientifico · ITHumanitas University · ITImperial College London · GB

Funding

European Research Council 692789
6 · The paper itself

Abstract

Interactions between the splicing machinery and RNA polymerase II increase protein-coding gene transcription. Similarly, exons and splicing signals of enhancer-generated long noncoding RNAs (elncRNAs) augment enhancer activity. However, elncRNAs are inefficiently spliced, suggesting that, compared with protein-coding genes, they contain qualitatively different exons with a limited ability to drive splicing. We show here that the inefficiently spliced first exons of elncRNAs as well as promoter-antisense long noncoding RNAs (pa-lncRNAs) in human and mouse cells trigger a transcription termination checkpoint that requires WDR82, an RNA polymerase II-binding protein, and its RNA-binding partner of previously unknown function, ZC3H4. We propose that the first exons of elncRNAs and pa-lncRNAs are an intrinsic component of a regulatory mechanism that, on the one hand, maximizes the activity of these cis-regulatory elements by recruiting the splicing machinery and, on the other, contains elements that suppress pervasive extragenic transcription.

Indexed as

Transcription, GeneticAlternative SplicingAnimalsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsExonsHumansMicePromoter Regions, GeneticRegulatory Sequences, Nucleic AcidRNA, AntisenseRNA, Long NoncodingRNA, MessengerRNA Polymerase IIRNA SplicingChromosomal Proteins, Non-HistoneDNA-Binding ProteinsRNA, AntisenseRNA, Long NoncodingRNA, MessengerRNA Polymerase IIWDR82 protein, humanZC3H4 protein, mouse

Identifiers

PMID33767452
PMCPMC7610630
OpenAlexW3138725889

What OpenQuestion holds

Textmetadata
LicenceTDM
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.