Evidence map›Paper›PMID 27044869›Full record

ArticleMolecular and cellular biology2016

Endogenous Hot Spots of De Novo Telomere Addition in the Yeast Genome Contain Proximal Enhancers That Bind Cdc13.

Udochukwu C Obodo, Esther A Epum, Margaret H Platts, Jacob Seloff, Nicole A Dahlson, Stoycho M Velkovsky, Shira R Paul, Katherine L Friedman

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Interstitial telomeric sequences promote gross chromosomal rearrangement via multiple mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. A comprehensive map of hotspots of de novo telomere addition inbioRxiv : the preprint server for biology · 2023
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. 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

8 authors.

Udochukwu C ObodoDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA.
Esther A EpumDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA.
Margaret H PlattsDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA.
Jacob SeloffDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA.
Nicole A DahlsonDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA.
Stoycho M VelkovskyDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA.
Shira R PaulDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA.
Katherine L FriedmanDepartment of Biological Sciences, Vanderbilt University, Nashville, Tennessee, USA katherine.friedman@vanderbilt.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA double-strand breaks (DSBs) pose a threat to genome stability and are repaired through multiple mechanisms. Rarely, telomerase, the enzyme that maintains telomeres, acts upon a DSB in a mutagenic process termed telomere healing. The probability of telomere addition is increased at specific genomic sequences termed sites of repair-associated telomere addition (SiRTAs). By monitoring repair of an induced DSB, we show that SiRTAs on chromosomes V and IX share a bipartite structure in which a core sequence (Core) is directly targeted by telomerase, while a proximal sequence (Stim) enhances the probability of de novo telomere formation. The Stim and Core sequences are sufficient to confer a high frequency of telomere addition to an ectopic site. Cdc13, a single-stranded DNA binding protein that recruits telomerase to endogenous telomeres, is known to stimulate de novo telomere addition when artificially recruited to an induced DSB. Here we show that the ability of the Stim sequence to enhance de novo telomere addition correlates with its ability to bind Cdc13, indicating that natural sites at which telomere addition occurs at high frequency require binding by Cdc13 to a sequence 20 to 100 bp internal from the site at which telomerase acts to initiate de novo telomere addition.

Indexed as

Enhancer Elements, GeneticBinding SitesDNA Breaks, Double-StrandedDNA, FungalDNA RepairGenome, FungalSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTelomeraseTelomereTelomere-Binding ProteinsCdc13 protein, S cerevisiaeDNA, FungalSaccharomyces cerevisiae ProteinsTelomeraseTelomere-Binding Proteins

Identifiers

PMID27044869
PMCPMC4907100

What OpenQuestion holds

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Registered trials

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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.