Evidence map›Paper›PMID 16537895›Full record

ArticleMolecular and cellular biology2006

Evidence suggesting that Pif1 helicase functions in DNA replication with the Dna2 helicase/nuclease and DNA polymerase delta.

Martin E Budd, Clara C Reis, Stephanie Smith, Kyungjae Myung, Judith L Campbell

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

143 citing papers in PubMed, 201 citations in OpenAlex.

  1. Review
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  5. Interstitial telomeric sequences promote gross chromosomal rearrangement via multiple mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  15. Role and Regulation of Pif1 Family Helicases at the Replication Fork.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

83 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

5 authors at 3 institutions in 2 countries.

Martin E BuddBraun Laboratories, 147-75, California Institute of Technology, Pasadena, California 91125, USA.
Clara C Reis
Stephanie Smith
Kyungjae Myung
Judith L Campbell
California Institute of Technology · USNational Human Genome Research Institute · USInstituto Gulbenkian de Ciência · PT

Funding

Genome Instability in Cancer DevelopmentZ01HG012003 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI MYUNG, KYUNGJAE · 2003 to 2008
$3.0M
ENZYMATIC MECHANISMS OF DNA REPLICATIONR01GM025508 · NIGMS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI CAMPBELL, JUDITH L · 1985 to 2006
$2.5M
Intramural NIH HHSNIGMS NIH HHS GM25508NIGMS NIH HHS R01 GM025508
6 · The paper itself

Abstract

The precise machineries required for two aspects of eukaryotic DNA replication, Okazaki fragment processing (OFP) and telomere maintenance, are poorly understood. In this work, we present evidence that Saccharomyces cerevisiae Pif1 helicase plays a wider role in DNA replication than previously appreciated and that it likely functions in conjunction with Dna2 helicase/nuclease as a component of the OFP machinery. In addition, we show that Dna2, which is known to associate with telomeres in a cell-cycle-specific manner, may be a new component of the telomere replication apparatus. Specifically, we show that deletion of PIF1 suppresses the lethality of a DNA2-null mutant. The pif1delta dna2delta strain remains methylmethane sulfonate sensitive and temperature sensitive; however, these phenotypes can be suppressed by further deletion of a subunit of pol delta, POL32. Deletion of PIF1 also suppresses the cold-sensitive lethality and hydroxyurea sensitivity of the pol32delta strain. Dna2 is thought to function by cleaving long flaps that arise during OFP due to excessive strand displacement by pol delta and/or by an as yet unidentified helicase. Thus, suppression of dna2delta can be rationalized if deletion of POL32 and/or PIF1 results in a reduction in long flaps that require Dna2 for processing. We further show that deletion of DNA2 suppresses the long-telomere phenotype and the high rate of formation of gross chromosomal rearrangements in pif1Delta mutants, suggesting a role for Dna2 in telomere elongation in the absence of Pif1.

Indexed as

DNA ReplicationAdenosine TriphosphatasesCell Cycle ProteinsCell NucleusCheckpoint Kinase 2DNA DamageDNA HelicasesDNA Polymerase IIIGene DeletionGenes, FungalMethyl MethanesulfonateMitochondriaModels, BiologicalMutationProtein BindingProtein Serine-Threonine KinasesAdenosine TriphosphatasesCell Cycle ProteinsCheckpoint Kinase 2DNA2 protein, S cerevisiaeDNA HelicasesDNA Polymerase IIIMethyl MethanesulfonatePIF1 protein, S cerevisiaeProtein Serine-Threonine KinasesRAD53 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTelomerase

Identifiers

PMID16537895
PMCPMC1430326
OpenAlexW2100310707

What OpenQuestion holds

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Registered trials

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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.