Evidence map›Paper›PMID 32001709›Full record

ArticleNature communications2020

Molecular signatures of aneuploidy-driven adaptive evolution.

Alaattin Kaya, Marco Mariotti, Alexander Tyshkovskiy, Xuming Zhou, Michelle L Hulke, Siming Ma, Maxim V Gerashchenko, Amnon Koren, Vadim N Gladyshev

Abstract read
In one paragraph

Article in Nature communications, 2020. 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

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

19 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
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  5. Article
  6. Review
  7. Article
  8. Targeting chromosomal instability in patients with cancer.Nature reviews. Clinical oncology · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Effects of aneuploidy on cell behaviour and function.Nature reviews. Molecular cell biology · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. 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

9 authors.

Alaattin Kaya *Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.ORCID http://orcid.org/0000-0002-6132-5197
Marco Mariotti *Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.ORCID http://orcid.org/0000-0002-7411-4161
Alexander TyshkovskiyDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.ORCID http://orcid.org/0000-0002-6215-190X
Xuming ZhouDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
Michelle L HulkeCornell University Department of Molecular Biology and Genetics, 526 Campus Road, Ithaca, NY, 14853, USA.
Siming MaDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
Maxim V GerashchenkoDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.ORCID http://orcid.org/0000-0001-8396-2202
Amnon KorenCornell University Department of Molecular Biology and Genetics, 526 Campus Road, Ithaca, NY, 14853, USA.
Vadim N GladyshevDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA. vgladyshev@rics.bwh.harvard.edu.

Funding

Functions of thioredoxin reductases and their targetsR37GM065204 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI GLADYSHEV, VADIM N. · 2011 to 2020
$4.0M
NIGMS NIH HHS R37 GM065204
6 · The paper itself

Abstract

Alteration of normal ploidy (aneuploidy) can have a number of opposing effects, such as unbalancing protein abundances and inhibiting cell growth but also accelerating genetic diversification and rapid adaptation. The interplay of these detrimental and beneficial effects remains puzzling. Here, to understand how cells develop tolerance to aneuploidy, we subject disomic (i.e. with an extra chromosome copy) strains of yeast to long-term experimental evolution under strong selection, by forcing disomy maintenance and daily population dilution. We characterize mutations, karyotype alterations and gene expression changes, and dissect the associated molecular strategies. Cells with different extra chromosomes accumulated mutations at distinct rates and displayed diverse adaptive events. They tended to evolve towards normal ploidy through chromosomal DNA loss and gene expression changes. We identify genes with recurrent mutations and altered expression in multiple lines, revealing a variant that improves growth under genotoxic stresses. These findings support rapid evolvability of disomic strains that can be used to characterize fitness effects of mutations under different stress conditions.

Indexed as

AneuploidyEvolution, MolecularAdaptation, PhysiologicalAllelesDNA DamageGene DosageGene Expression Regulation, FungalGene Regulatory NetworksGenome, FungalKaryotypeMutationPhenotypePromoter Regions, GeneticSaccharomyces cerevisiaeTranscription, Genetic

Identifiers

PMID32001709
PMCPMC6992709

What OpenQuestion holds

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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.