Evidence map›Paper›PMID 24835988›Full record

ArticleCell reports2014

Interplay between nonsense-mediated mRNA decay and DNA damage response pathways reveals that Stn1 and Ten1 are the key CST telomere-cap components.

Eva-Maria Holstein, Kate R M Clark, David Lydall

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-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

14 citing papers in PubMed, 23 citations in OpenAlex.

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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.

Eva-Maria HolsteinInstitute for Cell and Molecular Biosciences, Newcastle University Medical School, Newcastle upon Tyne NE2 4HH, UK.
Kate R M ClarkInstitute for Cell and Molecular Biosciences, Newcastle University Medical School, Newcastle upon Tyne NE2 4HH, UK.
David LydallInstitute for Cell and Molecular Biosciences, Newcastle University Medical School, Newcastle upon Tyne NE2 4HH, UK. Electronic address: david.lydall@newcastle.ac.uk.
Newcastle University · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F006039/1Biotechnology and Biological Sciences Research Council BBF016980/1Cancer Research UK 13314Medical Research Council MR/L001284/1Wellcome TrustWellcome Trust WT093088MA
6 · The paper itself

Abstract

A large and diverse set of proteins, including CST complex, nonsense mediated decay (NMD), and DNA damage response (DDR) proteins, play important roles at the telomere in mammals and yeast. Here, we report that NMD, like the DDR, affects single-stranded DNA (ssDNA) production at uncapped telomeres. Remarkably, we find that the requirement for Cdc13, one of the components of CST, can be efficiently bypassed when aspects of DDR and NMD pathways are inactivated. However, identical genetic interventions do not bypass the need for Stn1 and Ten1, the partners of Cdc13. We show that disabling NMD alters the stoichiometry of CST components at telomeres and permits Stn1 to bind telomeres in the absence of Cdc13. Our data support a model that Stn1 and Ten1 can function in a Cdc13-independent manner and have implications for the function of CST components across eukaryotes.

Indexed as

DNA DamageNonsense Mediated mRNA DecayCell Cycle ProteinsChromosomal Proteins, Non-HistoneDNA, Single-StrandedProtein BindingProtein Structure, SecondaryRNA, MessengerSaccharomyces cerevisiae ProteinsTelomereTelomere-Binding ProteinsYeastsCell Cycle ProteinsChromosomal Proteins, Non-HistoneDNA, Single-StrandedRNA, MessengerSaccharomyces cerevisiae ProteinsStn1 protein, S cerevisiaeTelomere-Binding ProteinsTEN1 protein, S cerevisiae

Identifiers

PMID24835988
PMCPMC4518466
OpenAlexW2011287318

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.