Evidence map›Paper›PMID 29216371›Full record

ArticleNucleic acids research2018

Fission yeast Ccq1 is a modulator of telomerase activity.

Christine A Armstrong, Vera Moiseeva, Laura C Collopy, Siân R Pearson, Tomalika R Ullah, Shidong T Xi, Jennifer Martin, Shaan Subramaniam, Sara Marelli, Hanna Amelina and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 17 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

11 authors at 1 institution in 1 country.

Christine A ArmstrongChromosome Maintenance Group, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Vera MoiseevaChromosome Maintenance Group, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Laura C CollopyChromosome Maintenance Group, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Siân R PearsonChromosome Maintenance Group, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Tomalika R UllahChromosome Maintenance Group, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Shidong T XiChromosome Maintenance Group, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Jennifer MartinChromosome Maintenance Group, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Shaan SubramaniamChromosome Maintenance Group, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Sara MarelliChromosome Maintenance Group, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Hanna AmelinaChromosome Maintenance Group, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Kazunori TomitaChromosome Maintenance Group, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
University College London · GB

Funding

Cancer Research UK 12097European Research Council 281722
6 · The paper itself

Abstract

Shelterin, the telomeric protein complex, plays a crucial role in telomere homeostasis. In fission yeast, telomerase is recruited to chromosome ends by the shelterin component Tpz1 and its binding partner Ccq1, where telomerase binds to the 3' overhang to add telomeric repeats. Recruitment is initiated by the interaction of Ccq1 with the telomerase subunit Est1. However, how telomerase is released following elongation remains to be established. Here, we show that Ccq1 also has a role in the suppression of telomere elongation, when coupled with the Clr4 histone H3 methyl-transferase complex and the Clr3 histone deacetylase and nucleosome remodelling complex, SHREC. We have dissected the functions of Ccq1 by establishing a Ccq1-Est1 fusion system, which bypasses the telomerase recruitment step. We demonstrate that Ccq1 forms two distinct complexes for positive and negative telomerase regulation, with Est1 and Clr3 respectively. The negative form of Ccq1 promotes dissociation of Ccq1-telomerase from Tpz1, thereby restricting local telomerase activity. The Clr4 complex also has a negative regulation activity with Ccq1, independently of SHREC. Thus, we propose a model in which Ccq1-Est1 recruits telomerase to mediate telomere extension, whilst elongated telomeric DNA recruits Ccq1 with the chromatin-remodelling complexes, which in turn releases telomerase from the telomere.

Indexed as

Telomere HomeostasisCarrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsHistone-Lysine N-MethyltransferaseMethyltransferasesModels, MolecularMutationProtein BindingProtein DomainsSchizosaccharomycesSchizosaccharomyces pombe ProteinsTelomeraseCarrier ProteinsCcq1 protein, S pombeCell Cycle ProteinsClr3 protein, S pombeclr4 protein, S pombeDNA-Binding ProteinsEST1 protein, S pombeHistone-Lysine N-MethyltransferaseMethyltransferasesSchizosaccharomyces pombe ProteinsTelomeraseTpz1 protein, S pombe

Identifiers

PMID29216371
PMCPMC5778466
OpenAlexW2775029631

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.