Evidence map›Paper›PMID 25931610›Full record

ArticleGenome biology and evolution2015

The evolutionary fate of alternatively spliced homologous exons after gene duplication.

Federico Abascal, Michael L Tress, Alfonso Valencia

Abstract read
In one paragraph

Article in Genome biology and evolution, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

19 citing papers in PubMed.

  1. Ancestral intronic splicing regulatory elements in the SCNbioRxiv : the preprint server for biology · 2026
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  2. Review
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  15. Review
  16. The ribosome-engaged landscape of alternative splicing.Nature structural & molecular biology · 2016
    Article
  17. Article
  18. Article
  19. 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

3 authors.

Federico AbascalStructural Biology and Biocomputing Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain fabascal@cnio.es mtress@cnio.es.
Michael L TressStructural Biology and Biocomputing Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain fabascal@cnio.es mtress@cnio.es.
Alfonso ValenciaStructural Biology and Biocomputing Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.

Funding

GENCODE Resource ProjectU41HG007234 · NHGRI · SANGER INSTITUTE · PI FLICEK, PAUL · 2013 to 2020
$20.3M
NHGRI NIH HHS U41 HG007234
6 · The paper itself

Abstract

Alternative splicing and gene duplication are the two main processes responsible for expanding protein functional diversity. Although gene duplication can generate new genes and alternative splicing can introduce variation through alternative gene products, the interplay between the two processes is complex and poorly understood. Here, we have carried out a study of the evolution of alternatively spliced exons after gene duplication to better understand the interaction between the two processes. We created a manually curated set of 97 human genes with mutually exclusively spliced homologous exons and analyzed the evolution of these exons across five distantly related vertebrates (lamprey, spotted gar, zebrafish, fugu, and coelacanth). Most of these exons had an ancient origin (more than 400 Ma). We found examples supporting two extreme evolutionary models for the behaviour of homologous axons after gene duplication. We observed 11 events in which gene duplication was accompanied by splice isoform separation, that is, each paralog specifically conserved just one distinct ancestral homologous exon. At other extreme, we identified genes in which the homologous exons were always conserved within paralogs, suggesting that the alternative splicing event cannot easily be separated from the function in these genes. That many homologous exons fall in between these two extremes highlights the diversity of biological systems and suggests that the subtle balance between alternative splicing and gene duplication is adjusted to the specific cellular context of each gene.

Indexed as

Alternative SplicingEvolution, MolecularExonsGene DuplicationAmino Acid SequenceAnimalsBase SequenceCalcium ChannelsConserved SequenceHumansPhylogenyProtein IsoformsSequence AlignmentVertebratesCalcium ChannelsProtein Isoformsalternative splicinggene duplicationhomologous exonsprotein diversitysubfunctionalization

Identifiers

PMID25931610
PMCPMC4494069

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Registered trials

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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.