Evidence map›Paper›PMID 26244544›Full record

ArticlePLoS genetics2015

The Evolutionary Potential of Phenotypic Mutations.

Hayato Yanagida, Ariel Gispan, Noam Kadouri, Shelly Rozen, Michal Sharon, Naama Barkai, Dan S Tawfik

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
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  6. Exploring the expanse between theoretical questions and experimental approaches in the modern study of evolvability.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2023
    Article
  7. Computational Evaluation of Peroxisomal Targeting Signals in Metazoa.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  8. Phenotypic mutations contribute to protein diversity and shape protein evolution.Protein science : a publication of the Protein Society · 2022
    Review
  9. Mechanisms of protein evolution.Protein science : a publication of the Protein Society · 2022
    Review
  10. Retention of duplicated genes in evolution.Trends in genetics : TIG · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. The causes of evolvability and their evolution.Nature reviews. Genetics · 2019
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Hayato YanagidaDepartment of Biological Chemistry, Weizmann Institute of Science, Rehovot, Israel.
Ariel GispanDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Noam KadouriDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Shelly RozenDepartment of Biological Chemistry, Weizmann Institute of Science, Rehovot, Israel.
Michal SharonDepartment of Biological Chemistry, Weizmann Institute of Science, Rehovot, Israel.
Naama BarkaiDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Dan S TawfikDepartment of Biological Chemistry, Weizmann Institute of Science, Rehovot, Israel.
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Errors in protein synthesis, so-called phenotypic mutations, are orders-of-magnitude more frequent than genetic mutations. Here, we provide direct evidence that alternative protein forms and phenotypic variability derived from translational errors paved the path to genetic, evolutionary adaptations via gene duplication. We explored the evolutionary origins of Saccharomyces cerevisiae IDP3 - an NADP-dependent isocitrate dehydrogenase mediating fatty acids ß-oxidation in the peroxisome. Following the yeast whole genome duplication, IDP3 diverged from a cytosolic ancestral gene by acquisition of a C-terminal peroxisomal targeting signal. We discovered that the pre-duplicated cytosolic IDPs are partially localized to the peroxisome owing to +1 translational frameshifts that bypass the stop codon and unveil cryptic peroxisomal targeting signals within the 3'-UTR. Exploring putative cryptic signals in all 3'-UTRs of yeast genomes, we found that other enzymes related to NADPH production such as pyruvate carboxylase 1 (PYC1) might be prone to peroxisomal localization via cryptic signals. Using laboratory evolution we found that these translational frameshifts are rapidly imprinted via genetic single base deletions occurring within the very same gene location. Further, as exemplified here, the sequences that promote translational frameshifts are also more prone to genetic deletions. Thus, genotypes conferring higher phenotypic variability not only meet immediate challenges by unveiling cryptic 3'-UTR sequences, but also boost the potential for future genetic adaptations.

Indexed as

Evolution, MolecularAmino Acid SequenceBase SequenceFrameshift MutationGene DuplicationIsocitrate DehydrogenaseMolecular Sequence DataMutationPeroxisomesPhenotypeProtein TransportSaccharomyces cerevisiaeIsocitrate Dehydrogenaseisocitrate dehydrogenase (NADP+)

Identifiers

PMID26244544
PMCPMC4526572
OpenAlexW1495276091

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.