Evidence map›Paper›PMID 21901113›Full record

ArticlePLoS genetics2011

Natural polymorphism in BUL2 links cellular amino acid availability with chronological aging and telomere maintenance in yeast.

Elizabeth X Kwan, Eric Foss, Leonid Kruglyak, Antonio Bedalov

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2011. 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
0.6field-weighted citation impact, top 41% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Polymorphism ofInternational journal of molecular sciences · 2023
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Natural variation of chronological aging in theNPJ aging and mechanisms of disease · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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.

Elizabeth X KwanClinical Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
Eric Foss
Leonid Kruglyak
Antonio Bedalov
Fred Hutch Cancer Center · USPrinceton University · USUniversity of Washington · US

Funding

University of Washington Nathan Shock Center of Excellence in the Basic Biology of AgingP30AG013280 · NIA · UNIVERSITY OF WASHINGTON · PI David J. Marcinek, Jessica E Young · 1995 to 2026
$27.1M
Seattle Cancer and Aging ProgramP20CA103728 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI RABINOVITCH, PETER S · 2003 to 2007
$3.4M
VIRAL ONCOLOGYT32CA009229 · NCI · UNIVERSITY OF WASHINGTON · PI LINIAL, MAXINE L · 1985 to 2007
$3.0M
Development of cambinol analogues as antilymphoma agentsR01CA129132 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BEDALOV, ANTONIO · 2008 to 2012
$1.8M
NCI NIH HHS CA103728-03NCI NIH HHS CA129132NCI NIH HHS P20 CA103728NCI NIH HHS R01 CA129132NCI NIH HHS T32 CA009229NCI NIH HHS T32 CA09229NIA NIH HHS 2P30AG013280-16NIA NIH HHS P30 AG013280
6 · The paper itself

Abstract

Aging and longevity are considered to be highly complex genetic traits. In order to gain insight into aging as a polygenic trait, we employed an outbred Saccharomyces cerevisiae model, generated by crossing a vineyard strain RM11 and a laboratory strain S288c, to identify quantitative trait loci that control chronological lifespan. Among the major loci that regulate chronological lifespan in this cross, one genetic linkage was found to be congruent with a previously mapped locus that controls telomere length variation. We found that a single nucleotide polymorphism in BUL2, encoding a component of an ubiquitin ligase complex involved in trafficking of amino acid permeases, controls chronological lifespan and telomere length as well as amino acid uptake. Cellular amino acid availability changes conferred by the BUL2 polymorphism alter telomere length by modulating activity of a transcription factor Gln3. Among the GLN3 transcriptional targets relevant to this phenotype, we identified Wtm1, whose upregulation promotes nuclear retention of ribonucleotide reductase (RNR) components and inhibits the assembly of the RNR enzyme complex during S-phase. Inhibition of RNR is one of the mechanisms by which Gln3 modulates telomere length. Identification of a polymorphism in BUL2 in this outbred yeast population revealed a link among cellular amino acid availability, chronological lifespan, and telomere length control.

Indexed as

Adaptor Proteins, Signal TransducingAgingAmino AcidsAmino Acid SequenceAmino Acid Transport SystemsMolecular Sequence DataPolymorphism, GeneticQuantitative Trait LociRepressor ProteinsRibonucleotide ReductasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsS PhaseTelomereTranscription FactorsUbiquitin-Protein Ligase ComplexesAdaptor Proteins, Signal TransducingAmino AcidsAmino Acid Transport SystemsBUL2 protein, S cerevisiaeGLN3 protein, S cerevisiaeRepressor ProteinsRibonucleotide ReductasesRnr1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTranscription FactorsUbiquitin-Protein Ligase ComplexesWtm1 protein, S cerevisiae

Identifiers

PMID21901113
PMCPMC3161923
OpenAlexW1995171819

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.