Evidence map›Paper›PMID 19704012›Full record

ArticleGenetics2009

Telomerase is essential to alleviate pif1-induced replication stress at telomeres.

Michael Chang, Brian Luke, Claudine Kraft, Zhijian Li, Matthias Peter, Joachim Lingner, Rodney Rothstein

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Telomere maintenance and the DNA damage response: a paradoxical alliance.Frontiers in cell and developmental biology · 2024
    Article
  5. Role and Regulation of Pif1 Family Helicases at the Replication Fork.International journal of molecular sciences · 2022
    Review
  6. Overcoming stochastic variations in culture variables to quantify and compare growth curve data.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021
    Article
  7. Lysine acetylation regulates the activity of nuclear Pif1.The Journal of biological chemistry · 2020
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Structure and function of Pif1 helicase.Biochemical Society transactions · 2017
    Review
  13. Article
  14. Pif1 is a force-regulated helicase.Nucleic acids research · 2016
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

7 authors at 3 institutions in 3 countries.

Michael ChangDepartment of Genetics, Columbia University Medical Center, New York, New York 10032, USA. mc3096@columbia.edu
Brian Luke
Claudine Kraft
Zhijian Li
Matthias Peter
Joachim Lingner
Rodney Rothstein
École Polytechnique Fédérale de Lausanne · CHColumbia University Irving Medical Center · USUniversity of Toronto · CA

Funding

Genetics of the formation of repair &reombination fociR01GM067055 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ROTHSTEIN, RODNEY J. · 2003 to 2014
$4.3M
Using synthetic dosage lethality to screen for novel anti-tumor targetsR33CA125520 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ROTHSTEIN, RODNEY J. · 2007 to 2009
$1.0M
CIHRNCI NIH HHS CA125520NCI NIH HHS R33 CA125520NIGMS NIH HHS GM67055NIGMS NIH HHS R01 GM067055
6 · The paper itself

Abstract

Pif1, an evolutionarily conserved helicase, negatively regulates telomere length by removing telomerase from chromosome ends. Pif1 has also been implicated in DNA replication processes such as Okazaki fragment maturation and replication fork pausing. We find that overexpression of Saccharomyces cervisiae PIF1 results in dose-dependent growth inhibition. Strong overexpression causes relocalization of the DNA damage response factors Rfa1 and Mre11 into nuclear foci and activation of the Rad53 DNA damage checkpoint kinase, indicating that the toxicity is caused by accumulation of DNA damage. We screened the complete set of approximately 4800 haploid gene deletion mutants and found that moderate overexpression of PIF1, which is only mildly toxic on its own, causes growth defects in strains with mutations in genes involved in DNA replication and the DNA damage response. Interestingly, we find that telomerase-deficient strains are also sensitive to PIF1 overexpression. Our data are consistent with a model whereby increased levels of Pif1 interfere with DNA replication, causing collapsed replication forks. At chromosome ends, collapsed forks result in truncated telomeres that must be rapidly elongated by telomerase to maintain viability.

Indexed as

Cell Cycle ProteinsCell DivisionCheckpoint Kinase 2DNA Breaks, Single-StrandedDNA DamageDNA HelicasesDNA RepairDNA ReplicationEndodeoxyribonucleasesExodeoxyribonucleasesGene Expression Regulation, FungalImmunoblottingLuminescent ProteinsMicroscopy, FluorescenceMutationProtein Serine-Threonine KinasesCell Cycle ProteinsCheckpoint Kinase 2DNA HelicasesEndodeoxyribonucleasesExodeoxyribonucleasesLuminescent ProteinsMRE11 protein, S cerevisiaePIF1 protein, S cerevisiaeProtein Serine-Threonine KinasesRAD53 protein, S cerevisiaeReplication Protein ARFA1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTelomerase

Identifiers

PMID19704012
PMCPMC2778976
OpenAlexW2120403234

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.