Evidence map›Paper›PMID 19214189›Full record

ArticleThe EMBO journal2009

Sgs1 function in the repair of DNA replication intermediates is separable from its role in homologous recombinational repair.

Kara A Bernstein, Erika Shor, Ivana Sunjevaric, Marco Fumasoni, Rebecca C Burgess, Marco Foiani, Dana Branzei, Rodney Rothstein

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 69 citations in OpenAlex.

  1. A multispecies toolkit ofProceedings of the National Academy of Sciences of the United States of America · 2026
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  16. BothAIMS genetics · 2017
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  20. Mechanism of DNA damage tolerance.World journal of biological chemistry · 2015
    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

8 authors at 3 institutions in 2 countries.

Kara A BernsteinDepartment of Genetics & Development, Columbia University Medical Center, New York, NY 10032, USA.
Erika Shor
Ivana Sunjevaric
Marco Fumasoni
Rebecca C Burgess
Marco Foiani
Dana Branzei
Rodney Rothstein
Columbia University Irving Medical Center · USUniversity of Milan · ITFIRC Institute of Molecular Oncology · IT

Funding

Mechanism of spontaneous and DSB-induced repairR37GM050237 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ROTHSTEIN, RODNEY J. · 2005 to 2014
$6.0M
Genetics of the formation of repair &reombination fociR01GM067055 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ROTHSTEIN, RODNEY J. · 2003 to 2014
$4.3M
MECHANISM OF SPONTANEOUS AND DSB-INDUCED REPAIRR01GM050237 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI ROTHSTEIN, RODNEY J. · 1993 to 2016
$3.0M
A Tripartite Approach to Elucidate Rdh54 functionF31GM073567 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BURGESS, REBECCA C · 2004 to 2007
$131k
Role of Sgs1, yeast Werner/Bloom homologue in DNA repairF32GM078840 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BERNSTEIN, KARA A · 2006 to 2009
$125k
NIGMS NIH HHS F31 GM073567NIGMS NIH HHS F32 GM078840NIGMS NIH HHS GM078840NIGMS NIH HHS GM50237NIGMS NIH HHS GM67055NIGMS NIH HHS GM73567NIGMS NIH HHS R01 GM050237NIGMS NIH HHS R01 GM067055NIGMS NIH HHS R37 GM050237
6 · The paper itself

Abstract

Mutations in human homologues of the bacterial RecQ helicase cause diseases leading to cancer predisposition and/or shortened lifespan (Werner, Bloom, and Rothmund-Thomson syndromes). The budding yeast Saccharomyces cerevisiae has one RecQ helicase, Sgs1, which functions with Top3 and Rmi1 in DNA repair. Here, we report separation-of-function alleles of SGS1 that suppress the slow growth of top3Delta and rmi1Delta cells similar to an SGS1 deletion, but are resistant to DNA damage similar to wild-type SGS1. In one allele, the second acidic region is deleted, and in the other, only a single aspartic acid residue 664 is deleted. sgs1-D664Delta, unlike sgs1Delta, neither disrupts DNA recombination nor has synthetic growth defects when combined with DNA repair mutants. However, during S phase, it accumulates replication-associated X-shaped structures at damaged replication forks. Furthermore, fluorescent microscopy reveals that the sgs1-D664Delta allele exhibits increased spontaneous RPA foci, suggesting that the persistent X-structures may contain single-stranded DNA. Taken together, these results suggest that the Sgs1 function in repair of DNA replication intermediates can be uncoupled from its role in homologous recombinational repair.

Indexed as

Recombination, GeneticDNA-Binding ProteinsDNA, FungalDNA RepairDNA ReplicationMicroscopy, FluorescenceMutationPhenotypeRecQ HelicasesReplication Protein ASaccharomyces cerevisiae ProteinsTranscription FactorsDNA-Binding ProteinsDNA, FungalRecQ HelicasesReplication Protein ARFA1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSGS1 protein, S cerevisiaeTranscription Factors

Identifiers

PMID19214189
PMCPMC2670856
OpenAlexW2132481441

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.