Evidence map›Paper›PMID 34801008›Full record

ArticleBMC biology2021

Telomerase subunit Est2 marks internal sites that are prone to accumulate DNA damage.

Satyaprakash Pandey, Mona Hajikazemi, Theresa Zacheja, Stephanie Schalbetter, Matthew J Neale, Jonathan Baxter, Victor Guryev, Andreas Hofmann, Dieter W Heermann, Stefan A Juranek and 1 more

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. A comprehensive map of hotspots of de novo telomere addition inbioRxiv : the preprint server for biology · 2023
    Article
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 3 countries.

Satyaprakash Pandey *University of Groningen, University Medical Center Groningen, European Research Institute for the Biology of Ageing, 9713 AV, Groningen, Netherlands.
Mona Hajikazemi *Clinic of Internal Medicine III, Oncology, Hematology, Rheumatology and Clinical Immunology, University Hospital Bonn, Bonn, Germany.
Theresa ZachejaClinic of Internal Medicine III, Oncology, Hematology, Rheumatology and Clinical Immunology, University Hospital Bonn, Bonn, Germany.
Stephanie SchalbetterDepartment of Life Science, University of Sussex, Brighton, UK.
Matthew J NealeDepartment of Life Science, University of Sussex, Brighton, UK.
Jonathan BaxterDepartment of Life Science, University of Sussex, Brighton, UK.
Victor GuryevUniversity of Groningen, University Medical Center Groningen, European Research Institute for the Biology of Ageing, 9713 AV, Groningen, Netherlands.
Andreas HofmannInstitute for Theoretical Physics, University of Heidelberg, Philosophenweg 12, 69120, Heidelberg, Germany.
Dieter W HeermannInstitute for Theoretical Physics, University of Heidelberg, Philosophenweg 12, 69120, Heidelberg, Germany.
Stefan A JuranekClinic of Internal Medicine III, Oncology, Hematology, Rheumatology and Clinical Immunology, University Hospital Bonn, Bonn, Germany. stefan.juranek@ukbonn.de.
Katrin PaeschkeUniversity of Groningen, University Medical Center Groningen, European Research Institute for the Biology of Ageing, 9713 AV, Groningen, Netherlands. katrin.paeschke@ukbonn.de.ORCID http://orcid.org/0000-0003-3080-6745
University Hospital Bonn · DEUniversity Medical Center Groningen · NLUniversity of Sussex · GBHeidelberg University · DE

Funding

Telomere maintenance and replication fork progression in yeast and human cellsR35GM118279 · NIGMS · PRINCETON UNIVERSITY · PI ZAKIAN, VIRGINIA A. · 2016 to 2020
$4.5M
NIGMS NIH HHS R35 GM118279
6 · The paper itself

Abstract

backgroundThe main function of telomerase is at the telomeres but under adverse conditions telomerase can bind to internal regions causing deleterious effects as observed in cancer cells.

resultsBy mapping the global occupancy of the catalytic subunit of telomerase (Est2) in the budding yeast Saccharomyces cerevisiae, we reveal that it binds to multiple guanine-rich genomic loci, which we termed "non-telomeric binding sites" (NTBS). We characterize Est2 binding to NTBS. Contrary to telomeres, Est2 binds to NTBS in G1 and G2 phase independently of Est1 and Est3. The absence of Est1 and Est3 renders telomerase inactive at NTBS. However, upon global DNA damage, Est1 and Est3 join Est2 at NTBS and telomere addition can be observed indicating that Est2 occupancy marks NTBS regions as particular risks for genome stability.

conclusionsOur results provide a novel model of telomerase regulation in the cell cycle using internal regions as "parking spots" of Est2 but marking them as hotspots for telomere addition.

Indexed as

Saccharomyces cerevisiae ProteinsTelomeraseDNA DamageSaccharomyces cerevisiaeTelomereEST1 protein, S cerevisiaeEST3 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTelomeraseDNA damageGenome stabilityTelomeraseYeast

Identifiers

PMID34801008
PMCPMC8605574
OpenAlexW3216877104

What Socratic 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 Socratic graph.