Evidence map›Paper›PMID 21474074›Full record

ArticleMolecular cell2011

A common telomeric gene silencing assay is affected by nucleotide metabolism.

Marlies P Rossmann, Weijun Luo, Olga Tsaponina, Andrei Chabes, Bruce Stillman

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. A novel role of DOT1L in kidney diseases.Molecular biology reports · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. A SIR-independent role for cohesin in subtelomeric silencing and organization.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Proliferating cell nuclear antigen (PCNA) contributes to the high-order structure and stability of heterochromatin in Saccharomyces cerevisiae.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2017
    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

5 authors at 2 institutions in 2 countries.

Marlies P RossmannCold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
Weijun Luo
Olga Tsaponina
Andrei Chabes
Bruce Stillman
Cold Spring Harbor Laboratory · USUmeå University · SE

Funding

VIRAL TRANSACTIVATIONP01CA013106 · NCI · COLD SPRING HARBOR LABORATORY · PI William Richard McCombie · 1985 to 2026
$116.8M
REGULATION OF DNA REPLICATIONR01GM045436 · NIGMS · COLD SPRING HARBOR LABORATORY · PI STILLMAN, BRUCE W. · 1991 to 2025
$15.8M
NCI NIH HHS CA13106NCI NIH HHS P01 CA013106NIGMS NIH HHS GM45436NIGMS NIH HHS R01 GM045436
6 · The paper itself

Abstract

Telomere-associated position-effect variegation (TPEV) in budding yeast has been used as a model for understanding epigenetic inheritance and gene silencing. A widely used assay to identify mutants with improper TPEV employs the URA3 gene at the telomere of chromosome VII-L that can be counterselected with 5-fluoroorotic acid (5-FOA). 5-FOA resistance has been inferred to represent lack of transcription of URA3 and therefore to represent heterochromatin-induced gene silencing. For two genes implicated in telomere silencing, POL30 and DOT1, we show that the URA3 telomere reporter assay does not reflect their role in heterochromatin formation. Rather, an imbalance in ribonucleotide reductase (RNR), which is induced by 5-FOA, and the specific promoter of URA3 fused to ADH4 at telomere VII-L are jointly responsible for the variegated phenotype. We conclude that metabolic changes caused by the drug employed and certain mutants being studied are incompatible with the use of certain prototrophic markers for TPEV.

Indexed as

Gene SilencingAntigens, NuclearChromosomal Position EffectsGenes, FungalHistone-Lysine N-MethyltransferaseModels, GeneticMutationNuclear ProteinsOrotic AcidProliferating Cell Nuclear AntigenRibonucleotide ReductasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTelomere5-fluoroorotic acidAntigens, NuclearDot1 protein, S cerevisiaeHistone-Lysine N-MethyltransferaseNuclear ProteinsOrotic AcidPOL30 protein, S cerevisiaeProliferating Cell Nuclear AntigenRibonucleotide ReductasesSaccharomyces cerevisiae ProteinsURA3 protein, S cerevisiae

Identifiers

PMID21474074
PMCPMC3086572
OpenAlexW2009047390

What OpenQuestion holds

Textmetadata
LicenceTDM
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.