Evidence map›Paper›PMID 26897341›Full record

ArticleBMC evolutionary biology2016

Models for gene duplication when dosage balance works as a transition state to subsequent neo-or sub-functionalization.

Ashley I Teufel, Liang Liu, David A Liberles

Abstract read
In one paragraph

Article in BMC evolutionary biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Evolution of intrinsic disorder in eukaryotic proteins.Cellular and molecular life sciences : CMLS · 2017
    Review
  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

3 authors.

Ashley I TeufelDepartment of Biology and Center for Computational Genetics and Genomics, Temple University, Philadelphia, PA, 19122, USA. ateufel@uwyo.edu.
Liang LiuDepartment of Statistics, University of Georgia, Athens, GA, 30602, USA. lliu@uga.edu.
David A LiberlesDepartment of Biology and Center for Computational Genetics and Genomics, Temple University, Philadelphia, PA, 19122, USA. daliberles@temple.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDosage balance has been described as an important process for the retention of duplicate genes after whole genome duplication events. However, dosage balance is only a temporary mechanism for duplicate gene retention, as it ceases to function following the stochastic loss of interacting partners, as dosage balance itself is lost with this event. With the prolonged period of retention, on the other hand, there is the potential for the accumulation of substitutions which upon release from dosage balance constraints, can lead to either subsequent neo-functionalization or sub-functionalization. Mechanistic models developed to date for duplicate gene retention treat these processes independently, but do not describe dosage balance as a transition state to eventual functional change.

resultsHere a model for these processes (dosage plus neofunctionalization and dosage plus subfunctionalization) has been built within an existing framework. Because of the computational complexity of these models, a simpler modeling framework that captures the same information is also proposed. This model is integrated into a phylogenetic birth-death model, expanding the range of available models.

conclusionsIncluding further levels of biological reality in methods for gene tree/species tree reconciliation should not only increase the accuracy of estimates of the timing and evolutionary history of genes but can also offer insight into how genes and genomes evolve. These new models add to the tool box for characterizing mechanisms of duplicate gene retention probabilistically.

Indexed as

Gene DosageGene DuplicationModels, GeneticEvolution, MolecularGenes, DuplicateGenomePhylogeny

Identifiers

PMID26897341
PMCPMC4761171

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.