Evidence map›Paper›PMID 18272435›Full record

ArticleDNA repair2008

The genetic consequences of ablating helicase activity and the Top3 interaction domain of Sgs1.

Justin Weinstein, Rodney Rothstein

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  9. The dissolution of double Holliday junctions.Cold Spring Harbor perspectives in biology · 2014
    Review
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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

2 authors at 1 institution in 1 country.

Justin WeinsteinDepartment of Genetics & Development, Columbia University Medical Center, 701 West 168th Street, New York, NY 10032-2704, USA.
Rodney Rothstein
Columbia University Irving Medical Center · US

Funding

PREDOCTORAL TRAINING GRANT IN HUMAN GENETICS &DEVELOPMET32GM007088 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI SHEN, MICHAEL M. · 1985 to 2020
$7.1M
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
NIGMS NIH HHS GM07088NIGMS NIH HHS GM50237NIGMS NIH HHS R01 GM050237NIGMS NIH HHS R37 GM050237NIGMS NIH HHS T32 GM007088
6 · The paper itself

Abstract

Sgs1, the RecQ helicase homolog, and Top3, the type-IA topoisomerase, physically interact and are required for genomic stability in budding yeast. Similarly, topoisomerase III genes physically pair with homologs of SGS1 in humans that are involved in the cancer predisposition and premature aging diseases Bloom, Werner, and Rothmund-Thompson syndromes. In the absence of Top1 activity, sgs1 mutants are severely growth impaired. Here, we investigate the role of Sgs1 helicase activity and its N-terminal Top3 interaction domain by using an allele-replacement technique to integrate mutant alleles at the native SGS1 genomic locus. We compare the phenotype of helicase-defective (sgs1-hd) and N-terminal deletion (sgs1-NDelta) strains to wild-type and sgs1 null strains. Like the sgs1 null, sgs1-hd mutations suppress top3 slow growth, cause a growth defect in the absence of Srs2 helicase, and impair meiosis. However, for recombination and the synthetic interaction with top1Delta mutations, loss of helicase activity exhibits a less severe phenotype than the null. Interestingly, deletion of the Top3 interaction domain of Sgs1 causes a top3-like phenotype, and furthermore, this effect is dependent on helicase activity. These results suggest that the protein-protein interaction between these two DNA-metabolism enzymes, even in the absence of helicase activity, is important for their function in catalyzing specific changes in DNA topology.

Indexed as

Binding SitesMeiosisMutationPhenotypeProtein BindingRecombination, GeneticRecQ HelicasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsRecQ HelicasesSaccharomyces cerevisiae ProteinsSGS1 protein, S cerevisiaeTOP3 protein, S cerevisiae

Identifiers

PMID18272435
PMCPMC2359228
OpenAlexW2001843819

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.