Evidence map›Paper›PMID 21459050›Full record

ArticleDNA repair2011

Srs2 overexpression reveals a helicase-independent role at replication forks that requires diverse cell functions.

Ana María León Ortiz, Robert J D Reid, John C Dittmar, Rodney Rothstein, Alain Nicolas

Abstract read
In one paragraph

Article in DNA repair, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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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

5 authors at 2 institutions in 2 countries.

Ana María León OrtizRecombination and Genome Instability, Institut Curie Centre de Recherche, CNRS UMR, Université Pierre et Marie Curie, Paris, France. Ana-Maria.Leon@curie.fr
Robert J D Reid
John C Dittmar
Rodney Rothstein
Alain Nicolas
Columbia University Irving Medical Center · USCentre National de la Recherche Scientifique · FR

Funding

CELL, MOLECULAR AND DEVELOPMENTAL BIOLOGY OF CANCERT32CA009503 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI GAUTIER, JEAN · 1985 to 2016
$6.8M
CELLULAR AND MOLECULAR FOUNDATIONS OF BIOMEDICAL SCIENCET32GM008798 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI PRYWES, RON M · 2001 to 2018
$6.3M
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
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
PCR AND RECOMBINATION FOR GENOMIC ANALYSIS IN YEASTF32HG000193 · NHGRI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REID, ROBERT J · 1999 to 2001
$94k
RECOMBINATION DIRECTED CONSTRUCTION OF PORTABLE LIBRARYR01HG001620 · NHGRI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ROTHSTEIN, RODNEY J. · 1997 to 1999
–
NCI NIH HHS CA009503NCI NIH HHS CA125520NCI NIH HHS R33 CA125520NCI NIH HHS T32 CA009503NHGRI NIH HHS F32 HG000193NHGRI NIH HHS HG00193NHGRI NIH HHS HG01620NHGRI NIH HHS R01 HG001620NIGMS NIH HHS GM008798NIGMS NIH HHS GM50237NIGMS NIH HHS R01 GM050237NIGMS NIH HHS R37 GM050237NIGMS NIH HHS T32 GM008798
6 · The paper itself

Abstract

Srs2 is a 3'-5' DNA helicase that regulates many aspects of DNA metabolism in Saccharomyces cerevisiae. It is best known for its ability to counteract homologous recombination by dismantling Rad51 filaments, but is also involved in checkpoint activation, adaptation and recovery, and in resolution of late recombination intermediates. To further address its biological roles and uncover new genetic interactions, we examined the consequences of overexpressing SRS2 as well as two helicase-dead mutants, srs2-K41A and srs2-K41R, in the collection of 4827 yeast haploid deletion mutants. We identified 274 genes affecting a large variety of cellular functions that are required for cell growth when SRS2 or its mutants are overexpressed. Further analysis of these interactions reveals that Srs2 acts independently of its helicase function at replication forks likely through its recruitment by the sumoylated PCNA replication clamp. This helicase-independent function is responsible for the negative interactions with DNA metabolism genes and for the toxicity of SRS2 overexpression in many of the diverse cellular pathways revealed in our screens.

Indexed as

Cell CycleDNA HelicasesDNA ReplicationGene ExpressionGene Expression ProfilingGene Expression Regulation, FungalMicrobial ViabilityMutant ProteinsProliferating Cell Nuclear AntigenProtein BindingRad51 RecombinaseSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSumoylationDNA HelicasesMutant ProteinsProliferating Cell Nuclear AntigenRad51 RecombinaseSaccharomyces cerevisiae ProteinsSRS2 protein, S cerevisiae

Identifiers

PMID21459050
PMCPMC3084345
OpenAlexW2087603327

What OpenQuestion holds

Textmetadata
LicenceTDM
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.