Evidence map›Paper›PMID 7896088›Full record

ArticleGenetics1994

Mutational analysis defines a C-terminal tail domain of RAP1 essential for Telomeric silencing in Saccharomyces cerevisiae.

C Liu, X Mao, A J Lustig

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Genetics, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
1.7field-weighted citation impact, top 11% 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

50 citing papers in PubMed, 92 citations in OpenAlex.

  1. Review
  2. 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
  3. Article
  4. Regulation of Antigenic Variation byPathogens (Basel, Switzerland) · 2021
    Review
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  8. Review
  9. Article
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  12. Article
  13. Article
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  15. Article
  16. ELG1, a regulator of genome stability, has a role in telomere length regulation and in silencing.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  17. 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

3 authors at 1 institution in 1 country.

C LiuGraduate Program in Molecular Biology, Cornell University Graduate School of Medical Sciences, New York, New York 10021.
X Mao
A J Lustig
Cornell University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
NCI NIH HHS P30CA-08748
6 · The paper itself

Abstract

Alleles specifically defective in telomeric silencing were generated by in vitro mutagenesis of the yeast RAP1 gene. The most severe phenotypes occur with three mutations in the C-terminal 28 amino acids. Two of the alleles are nonsense mutations resulting in truncated repressor/activator protein 1 (RAP1) species lacking the C-terminal 25-28 amino acids; the third allele is a missense mutation within this region. These alleles define a novel 28-amino acid region, termed the C-terminal tail domain, that is essential for telomeric and HML silencing. Using site-directed mutagenesis, an 8-amino acid region (amino acids 818-825) that is essential for telomeric silencing has been localized within this domain. Further characterization of these alleles has indicated that the C-terminal tail domain also plays a role in telomere size control. The function of the C-terminal tail in telomere maintenance is not mediated through the RAP1 interacting factor RIF1: rap1 alleles defective in both the C-terminal tail and RIF1 interaction domains have additive effects on telomere length. Overproduction of SIR3, a dose-dependent enhancer of telomeric silencing, suppresses the telomeric silencing, but not length, phenotypes of a subset of C-terminal tail alleles. In contrast, an allele that truncates the terminal 28 amino acids of RAP1 is refractory to SIR3 overproduction. These results indicate that the C-terminal tail domain is required for SIR3-dependent enhancement of telomeric silencing. These data also suggest a distinct set of C-terminal requirements for telomere size control and telomeric silencing.

Indexed as

Gene Expression Regulation, FungalProtein Structure, TertiarySaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeTelomere-Binding ProteinsAllelesAmino Acid SequenceBase SequenceDNA-Binding ProteinsDNA, FungalDNA Mutational AnalysisFungal ProteinsGTP-Binding ProteinsMolecular Sequence DataMutagenesis, Site-DirectedPoint MutationDNA-Binding ProteinsDNA, FungalFungal ProteinsGTP-Binding Proteinsrap GTP-Binding ProteinsRepressor ProteinsRIF1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSIR3 protein, S cerevisiaeTelomere-Binding ProteinsTrans-Activators

Identifiers

PMID7896088
PMCPMC1206245
OpenAlexW1754822275

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.