Evidence map›Paper›PMID 23275878›Full record

ArticleG3 (Bethesda, Md.)2012

The enigmatic conservation of a Rap1 binding site in the Saccharomyces cerevisiae HMR-E silencer.

Leonid Teytelman, Erin A Osborne Nishimura, Bilge Özaydin, Michael B Eisen, Jasper Rine

Open access · goldAbstract read
In one paragraph

Article in G3 (Bethesda, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.1field-weighted citation impact, top 48% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Context-dependent function of the transcriptional regulator Rap1 in gene silencing and activation inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  2. Article
  3. Article
  4. Article
  5. Highly expressed loci are vulnerable to misleading ChIP localization of multiple unrelated proteins.Proceedings of the National Academy of Sciences of the United States of America · 2013
    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 1 country.

Leonid TeytelmanDepartment of Molecular and Cell Biology and California Institute for Quantitative Biosciences, University of California, Berkeley, California 94720-3220, USA.
Erin A Osborne Nishimura
Bilge Özaydin
Michael B Eisen
Jasper Rine
QB3 · USUniversity of California, Berkeley · US

Funding

GENETIC ANALYSIS OF THE GENES CONTROLLING A POSITIONR01GM031105 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI RINE, JASPER D · 1985 to 2020
$6.4M
Modeling the Evolution and Function of Drosophila cis-Regulatory ModulesR01HG002779 · NHGRI · UNIVERSITY OF CALIFORNIA BERKELEY · PI EISEN, MICHAEL BRUCE · 2003 to 2012
$5.3M
GENETIC ANALYSIS OF GENES CONTROLLING A POSITION EFFECTR37GM031105 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI RINE, JASPER D · 1999 to 2008
$3.5M
Howard Hughes Medical InstituteNHGRI NIH HHS HG002779NHGRI NIH HHS R01 HG002779NIGMS NIH HHS GM31105NIGMS NIH HHS R01 GM031105NIGMS NIH HHS R37 GM031105
6 · The paper itself

Abstract

Silencing at the HMR and HML loci in Saccharomyces cerevisiae requires recruitment of Sir proteins to the HML and HMR silencers. The silencers are regulatory sites flanking both loci and consisting of binding sites for the Rap1, Abf1, and ORC proteins, each of which also functions at hundreds of sites throughout the genome in processes unrelated to silencing. Interestingly, the sequence of the binding site for Rap1 at the silencers is distinct from the genome-wide binding profile of Rap1, being a weaker match to the consensus, and indeed is bound with low affinity relative to the consensus sequence. Remarkably, this low-affinity Rap1 binding site variant was conserved among silencers of the sensu stricto Saccharomyces species, maintained as a poor match to the Rap1 genome-wide consensus sequence in all of them. We tested multiple predictions about the possible role of this binding-site variant in silencing by substituting the native Rap1 binding site at the HMR-E silencer with the genome-wide consensus sequence for Rap1. Contrary to the predictions from the current models of Rap1, we found no influence of the Rap1 binding site version on the kinetics of establishing silencing, nor on the maintenance of silencing, nor the extent of silencing. We further explored implications of these findings with regard to prevention of ectopic silencing, and deduced that the selective pressure for the unprecedented conservation of this binding site variant may not be related to silencing.

Indexed as

Gene SilencingBinding SitesDNA-Binding ProteinsGenes, FungalGenetic LociOrigin Recognition ComplexSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsShelterin ComplexTelomere-Binding ProteinsTranscription FactorsABF1 protein, S cerevisiaeDNA-Binding ProteinsOrigin Recognition ComplexRAP1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsShelterin ComplexTelomere-Binding ProteinsTranscription FactorsgenomicsRap1sensu strictosilencingtranscription factors

Identifiers

PMID23275878
PMCPMC3516477
OpenAlexW2033901621

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.