Evidence map›Paper›PMID 19141478›Full record

ArticleGenes & development2008

Fission yeast Ccq1 is telomerase recruiter and local checkpoint controller.

Kazunori Tomita, Julia Promisel Cooper

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
–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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

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6 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Kazunori TomitaTelomere Biology Laboratory, Cancer Research UK, London WC2A 3PX, United Kingdom.
Julia Promisel Cooper
Cancer Research UK · GB

Funding

Cancer Research UK
6 · The paper itself

Abstract

Telomeres recruit telomerase and differentiate chromosome ends from sites of DNA damage. Although the DNA damage checkpoint PI3-kinases ATM and ATR localize to telomeres and promote telomerase activation, activation of their downstream checkpoint pathway targets is inhibited. Here, we show that the fission yeast telomeric protein Ccq1 is required for telomerase recruitment and inhibition of ATR target activation at telomeres. The loss of Ccq1 results in progressive telomere shortening and persistent ATR-dependent activation of Chk1. Unlike the checkpoint activation that follows loss of telomerase, this checkpoint activation occurs prior to detectable levels of critically short telomeres. When ccq1Delta telomeres do become critically short, activated Chk1 promotes an unusual homologous recombination-based telomere maintenance process. We find that the previously reported meiotic segregation defects of cells lacking Ccq1 stem from its role in telomere maintenance rather than from a role in formation of the meiotic bouquet. These findings demonstrate the existence of a novel telomerase recruitment factor that also serves to suppress local checkpoint activation.

Indexed as

Checkpoint Kinase 1Chromosomes, FungalGenes, cdcMeiosisMitosisProtein KinasesRecombination, GeneticSchizosaccharomycesSchizosaccharomyces pombe ProteinsSequence DeletionTelomeraseTelomereTelomere-Binding ProteinsCcq1 protein, S pombeCheckpoint Kinase 1Chk1 protein, S pombeProtein KinasesSchizosaccharomyces pombe Proteinstaz1 protein, S pombeTelomeraseTelomere-Binding Proteins

Identifiers

PMID19141478
PMCPMC2607071
OpenAlexW2120055220

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.