Evidence map›Paper›PMID 16816432›Full record

ArticleGenetics2006

The absence of Top3 reveals an interaction between the Sgs1 and Pif1 DNA helicases in Saccharomyces cerevisiae.

Marisa Wagner, Gavrielle Price, Rodney Rothstein

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Role and Regulation of Pif1 Family Helicases at the Replication Fork.International journal of molecular sciences · 2022
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. TheGenetics · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Cell biology of mitotic recombination.Cold Spring Harbor perspectives in biology · 2015
    Review
  17. Review
  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

3 authors at 1 institution in 1 country.

Marisa WagnerDepartment of Genetics and Development, College of Physicians and Surgeons, Columbia University, New York, New York 10032-2704, USA.
Gavrielle Price
Rodney Rothstein
Columbia University · US

Funding

Mechanism of spontaneous and DSB-induced repairR37GM050237 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ROTHSTEIN, RODNEY J. · 2005 to 2014
$6.0M
MECHANISM OF SPONTANEOUS AND DSB-INDUCED REPAIRR01GM050237 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI ROTHSTEIN, RODNEY J. · 1993 to 2016
$3.0M
EXPLORING THE INTERACTION BETWEEN SGS1 AND TOP3F32CA090047 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI WAGNER, MARISA · 2001 to 2004
$149k
NCI NIH HHS CA90047NCI NIH HHS F32 CA090047NIGMS NIH HHS GM50237NIGMS NIH HHS R01 GM050237NIGMS NIH HHS R37 GM050237
6 · The paper itself

Abstract

RecQ DNA helicases and Topo III topoisomerases have conserved genetic, physical, and functional interactions that are consistent with a model in which RecQ creates a recombination-dependent substrate that is resolved by Topo III. The phenotype associated with Topo III loss suggests that accumulation of a RecQ-created substrate is detrimental. In yeast, mutation of the TOP3 gene encoding Topo III causes pleiotropic defects that are suppressed by deletion of the RecQ homolog Sgs1. We searched for gene dosage suppressors of top3 and identified Pif1, a DNA helicase that acts with polarity opposite to that of Sgs1. Pif1 overexpression suppresses multiple top3 defects, but exacerbates sgs1 and sgs1 top3 defects. Furthermore, Pif1 helicase activity is essential in the absence of Top3 in an Sgs1-dependent manner. These data clearly demonstrate that Pif1 helicase activity is required to counteract Sgs1 helicase activity that has become uncoupled from Top3. Pif1 genetic interactions with the Sgs1-Top3 pathway are dependent upon homologous recombination. We also find that Pif1 is recruited to DNA repair foci and that the frequency of these foci is significantly increased in top3 mutants. Our results support a model in which Pif1 has a direct role in the prevention or repair of Sgs1-induced DNA damage that accumulates in top3 mutants.

Indexed as

DNA DamageDNA HelicasesDNA RepairDNA Topoisomerases, Type IGenes, LethalProtein Interaction MappingRecombination, GeneticRecQ HelicasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionDNA HelicasesDNA Topoisomerases, Type IPIF1 protein, S cerevisiaeRecQ HelicasesSaccharomyces cerevisiae ProteinsSGS1 protein, S cerevisiaeTOP3 protein, S cerevisiae

Identifiers

PMID16816432
PMCPMC1602079
OpenAlexW2158658867

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.