Evidence map›Paper›PMID 22377634›Full record

ArticleGenetics2012

A naturally thermolabile activity compromises genetic analysis of telomere function in Saccharomyces cerevisiae.

Margherita Paschini, Tasha B Toro, Johnathan W Lubin, Bari Braunstein-Ballew, Danna K Morris, Victoria Lundblad

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2012. 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
1.4field-weighted citation impact, top 21% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Investigating the role of G-quadruplexes atMicrobial cell (Graz, Austria) · 2022
    Article
  4. Article
  5. Article
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  8. Review
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  10. Single-stranded telomere-binding protein employs a dual rheostat for binding affinity and specificity that drives function.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Telomerase RNA stem terminus element affects template boundary element function, telomere sequence, and shelterin binding.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

Margherita PaschiniSalk Institute for Biological Studies, La Jolla, California 92037-1099, USA.
Tasha B Toro
Johnathan W Lubin
Bari Braunstein-Ballew
Danna K Morris
Victoria Lundblad
Salk Institute for Biological Studies · USUniversity of California, San Diego · USBaylor College of Medicine · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
DUAL ROLE FOR CDC13 IN YEAST TELOMERE FUNCTIONR01GM055867 · NIGMS · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI LUNDBLAD, VICTORIA · 1997 to 2004
$1.4M
NCI NIH HHS P30 CA014195NCI NIH HHS P30-CA014195NIGMS NIH HHS GM55867NIGMS NIH HHS R01 GM055867
6 · The paper itself

Abstract

The core assumption driving the use of conditional loss-of-function reagents such as temperature-sensitive mutations is that the resulting phenotype(s) are solely due to depletion of the mutant protein under nonpermissive conditions. However, prior published data, combined with observations presented here, challenge the generality of this assumption at least for telomere biology: for both wild-type yeast and strains bearing null mutations in telomere protein complexes, there is an additional phenotypic consequence when cells are grown above 34°. We propose that this synthetic phenotype is due to a naturally thermolabile activity that confers a telomere-specific defect, which we call the Tmp(-) phenotype. This prompted a re-examination of commonly used cdc13-ts and stn1-ts mutations, which indicates that these alleles are instead hypomorphic mutations that behave as apparent temperature-sensitive mutations due to the additive effects of the Tmp(-) phenotype. We therefore generated new cdc13-ts reagents, which are nonpermissive below 34°, to allow examination of cdc13-depleted phenotypes in the absence of this temperature-dependent defect. A return-to-viability experiment following prolonged incubation at 32°, 34°, and 36° with one of these new cdc13-ts alleles argues that the accelerated inviability previously observed at 36° in cdc13-1 rad9-Δ mutant strains is a consequence of the Tmp(-) phenotype. Although this study focused on telomere biology, viable null mutations that confer inviability at 36° have been identified for multiple cellular pathways. Thus, phenotypic analysis of other aspects of yeast biology may similarly be compromised at high temperatures by pathway-specific versions of the Tmp(-) phenotype.

Indexed as

TemperatureAllelesMicrobial ViabilityMutagenesisMutationPhenotypeProtein Structure, TertiarySaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTelomereTelomere ShorteningSaccharomyces cerevisiae Proteins

Identifiers

PMID22377634
PMCPMC3338272
OpenAlexW2107820972

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.