Evidence map›Paper›PMID 11805044›Full record

ArticleGenetics2002

Differential suppression of DNA repair deficiencies of Yeast rad50, mre11 and xrs2 mutants by EXO1 and TLC1 (the RNA component of telomerase).

L Kevin Lewis, G Karthikeyan, James W Westmoreland, Michael A Resnick

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

56 citing papers in PubMed, 92 citations in OpenAlex.

  1. Asymmetrical recognition and processing of double-strand breaks formed during DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  16. Ionizing irradiation-induced radical stress stalls live meiotic chromosome movements by altering the actin cytoskeleton.Proceedings of the National Academy of Sciences of the United States of America · 2013
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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

4 authors at 1 institution in 1 country.

L Kevin LewisLaboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA.
G Karthikeyan
James W Westmoreland
Michael A Resnick
National Institutes of Health · US

Funding

Double Strand Break Repair And RecombinationZIAES021016 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI MENENDEZ RENDON, DANIEL · 2009 to 2018
$5.6M
ENZYMES INVOLVED IN DNA REPAIR AND MEIOSISZ01ES021016 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI RESNICK, MICHAEL A · 1985 to 2008
$1.1M
6 · The paper itself

Abstract

Rad50, Mre11, and Xrs2 form a nuclease complex that functions in both nonhomologous end-joining (NHEJ) and recombinational repair of DNA double-strand breaks (DSBs). A search for highly expressed cDNAs that suppress the DNA repair deficiency of rad50 mutants yielded multiple isolates of two genes: EXO1 and TLC1. Overexpression of EXO1 or TLC1 increased the resistance of rad50, mre11, and xrs2 mutants to ionizing radiation and MMS, but did not increase resistance in strains defective in recombination (rad51, rad52, rad54, rad59) or NHEJ only (yku70, sir4). Increased Exo1 or TLC1 RNA did not alter checkpoint responses or restore NHEJ proficiency, but DNA repair defects of yku70 and rad27 (fen) mutants were differentially suppressed by the two genes. Overexpression of Exo1, but not mutant proteins containing substitutions in the conserved nuclease domain, increased recombination and suppressed HO and EcoRI endonuclease-induced killing of rad50 strains. exo1 rad50 mutants lacking both nuclease activities exhibited a high proportion of enlarged, G2-arrested cells and displayed a synergistic decrease in DSB-induced plasmid:chromosome recombination. These results support a model in which the nuclease activity of the Rad50/Mre11/Xrs2 complex is required for recombinational repair, but not NHEJ. We suggest that the 5'-3' exo activity of Exo1 is able to substitute for Rad50/Mre11/Xrs2 in rescission of specific classes of DSB end structures. Gene-specific suppression by TLC1, which encodes the RNA subunit of the yeast telomerase complex, demonstrates that components of telomerase can also impact on DSB repair pathways.

Indexed as

Antigens, NuclearDNA, FungalDNA HelicasesSaccharomyces cerevisiae ProteinsDNA-Binding ProteinsDNA RepairEndodeoxyribonucleasesExodeoxyribonucleasesFlap EndonucleasesFungal ProteinsKu AutoantigenNuclear ProteinsRecombination, GeneticRNA, FungalSaccharomyces cerevisiaeTelomeraseAntigens, NuclearDNA-Binding ProteinsDNA, FungalDNA HelicasesEndodeoxyribonucleasesexodeoxyribonuclease IExodeoxyribonucleasesFlap EndonucleasesFungal Proteinshigh affinity DNA-binding factor, S cerevisiaeKu AutoantigenMRE11 protein, S cerevisiaeNuclear ProteinsRAD27 protein, S cerevisiaeRAD50 protein, S cerevisiaeRNA, FungalSaccharomyces cerevisiae ProteinsTelomeraseXRCC5 protein, humanXrcc6 protein, humanXRS2 protein, S cerevisiaeYKU70 protein, S cerevisiae

Identifiers

PMID11805044
PMCPMC1461956
OpenAlexW2170445225

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.