Evidence map›Paper›PMID 28811464›Full record

ArticleNature communications2017

The origin of a primordial genome through spontaneous symmetry breaking.

Nobuto Takeuchi, Paulien Hogeweg, Kunihiko Kaneko

Abstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
  2. Origins of life: the possible and the actual.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Article
  3. Generalizing the central dogma as a cross-hierarchical principle of biology.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  4. Article
  5. The key role of cheaters in the persistence of cooperation.bioRxiv : the preprint server for biology · 2024
    Article
  6. Formation of human kinship structures depending on population size and cultural mutation rate.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Evolution of kinship structures driven by marriage tie and competition.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. Article
  17. Article
  18. Reduced Local Symmetry in Lithium Compound LiAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019
    Article
  19. Physical foundations of biological complexity.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  20. Review
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.

Nobuto TakeuchiDepartment of Basic Science, Graduate School of Arts and Sciences, University of Tokyo, Komaba 3-8-1, Meguro-ku, Tokyo, 153-8902, Japan. takeuchi@complex.c.u-tokyo.ac.jp.
Paulien HogewegTheoretical Biology and Bioinformatics Group, Utrecht University, Padualaan 8, 3584CH, Utrecht, The Netherlands.
Kunihiko KanekoDepartment of Basic Science, Graduate School of Arts and Sciences, University of Tokyo, Komaba 3-8-1, Meguro-ku, Tokyo, 153-8902, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The heredity of a cell is provided by a small number of non-catalytic templates-the genome. How did genomes originate? Here, we demonstrate the possibility that genome-like molecules arise from symmetry breaking between complementary strands of self-replicating molecules. Our model assumes a population of protocells, each containing a population of self-replicating catalytic molecules. The protocells evolve towards maximising the catalytic activities of the molecules to increase their growth rates. Conversely, the molecules evolve towards minimising their catalytic activities to increase their intracellular relative fitness. These conflicting tendencies induce the symmetry breaking, whereby one strand of the molecules remains catalytic and increases its copy number (enzyme-like molecules), whereas the other becomes non-catalytic and decreases its copy number (genome-like molecules). This asymmetry increases the equilibrium cellular fitness by decreasing mutation pressure and increasing intracellular genetic drift. These results implicate conflicting multilevel evolution as a key cause of the origin of genetic complexity.Early molecules of life likely served both as templates and catalysts, raising the question of how functionally distinct genomes and enzymes arose. Here, the authors show that conflict between evolution at the molecular and cellular levels can drive functional differentiation of the two strands of self-replicating molecules and lead to copy number differences between the two.

Indexed as

GenomeModels, GeneticArtificial CellsCatalysisEvolution, MolecularGenetic Drift

Identifiers

PMID28811464
PMCPMC5557888

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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.