Evidence map›Paper›PMID 22949655›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Sex, prions, and plasmids in yeast.

Amy C Kelly, Frank P Shewmaker, Dmitry Kryndushkin, Reed B Wickner

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.4field-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

46 citing papers in PubMed, 67 citations in OpenAlex.

  1. Yeast Prions: Discovery, Nature, Cellular Manipulation and Implication.Journal of microbiology and biotechnology · 2025
    Review
  2. Anti-Prion Systems in Saccharomyces cerevisiae.Journal of neurochemistry · 2025
    Review
  3. Article
  4. The [PSIMolecular biology of the cell · 2022
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Normal levels of ribosome-associated chaperones cure two groups of [PSI+] prion variants.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  14. Article
  15. How Do Yeast Cells Contend with Prions?International journal of molecular sciences · 2020
    Review
  16. Prions: Roles in Development and Adaptive Evolution.Journal of molecular evolution · 2020
    Review
  17. Review
  18. Anti-prion systems in yeast.The Journal of biological chemistry · 2019
    Review
  19. Article
  20. Nonsense-mediated mRNA decay factors cure most [PSI+] prion variants.Proceedings of the National Academy of Sciences of the United States of America · 2018
    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

4 authors at 3 institutions in 1 country.

Amy C KellyLaboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Frank P Shewmaker
Dmitry Kryndushkin
Reed B Wickner
Uniformed Services University of the Health Sciences · USNational Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Prions of Yeast and Anti-Prion SystemsZIADK024950 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI WICKNER, REED B. · 2009 to 2025
$25.2M
Intramural NIH HHS
6 · The paper itself

Abstract

Even deadly prions may be widespread in nature if they spread by infection faster than they kill off their hosts. The yeast prions [PSI+] and [URE3] (amyloids of Sup35p and Ure2p) were not found in 70 wild strains, while [PIN+] (amyloid of Rnq1p) was found in ∼16% of the same population. Yeast prion infection occurs only by mating, balancing the detrimental effects of carrying the prion. We estimated the frequency of outcross mating as about 1% of mitotic doublings from the known detriment of carrying the 2-μm DNA plasmid (∼1%) and its frequency in wild populations (38/70). We also estimated the fraction of total matings that are outcross matings (∼23-46%) from the fraction of heterozygosity at the highly polymorphic RNQ1 locus (∼46%). These results show that the detriment of carrying even the mildest forms of [PSI+], [URE3], or [PIN+] is greater than 1%. We find that Rnq1p polymorphisms in wild strains include several premature stop codon alleles that cannot propagate [PIN+] from the reference allele and others with several small deletions and point mutations which show a small transmission barrier. Wild strains carrying [PIN+] are far more likely to be heterozygous at RNQ1 and other loci than are [pin-] strains, probably reflecting its being a sexually transmitted disease. Because sequence differences are known to block prion propagation or ameliorate its pathogenic effects, we hypothesize that polymorphism of RNQ1 was selected to protect cells from detrimental effects of the [PIN+] prion.

Indexed as

Biological EvolutionSexAmyloidBase SequenceGenetics, PopulationMolecular Sequence DataMutationPlasmidsPrionsReproductionSaccharomyces cerevisiae ProteinsSelection, GeneticSequence Analysis, DNAYeastsAmyloidPrionsRNQ1 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID22949655
PMCPMC3479589
OpenAlexW2000878370

What OpenQuestion holds

Textmetadata
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.