Evidence map›Paper›PMID 21508669›Full record

ArticleCell cycle (Georgetown, Tex.)2011

Inviability of a DNA2 deletion mutant is due to the DNA damage checkpoint.

Martin E Budd, Igor A Antoshechkin, Clara Reis, Barbara J Wold, Judith L Campbell

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 43 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Martin E BuddCalifornia Institute of Technology, Pasadena, CA USA.
Igor A Antoshechkin
Clara Reis
Barbara J Wold
Judith L Campbell
California Institute of Technology · USCortech Solutions (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dna2 is a dual polarity exo/endonuclease, and 5' to 3' DNA helicase involved in Okazaki Fragment Processing (OFP) and Double-Strand Break (DSB) Repair. In yeast, DNA2 is an essential gene, as expected for a DNA replication protein. Suppression of the lethality of dna2Δ mutants has been found to occur by two mechanisms: overexpression of RAD27 (scFEN1) , encoding a 5' to 3' exo/endo nuclease that processes Okazaki fragments (OFs) for ligation, or deletion of PIF1, a 5' to 3' helicase involved in mitochondrial recombination, telomerase inhibition and OFP. Mapping of a novel, spontaneously arising suppressor of dna2Δ now reveals that mutation of rad9 and double mutation of rad9 mrc1 can also suppress the lethality of dna2Δ mutants. Interaction of dna2Δ and DNA damage checkpoint mutations provides insight as to why dna2Δ is lethal but rad27Δ is not, even though evidence shows that Rad27 (ScFEN1) processes most of the Okazaki fragments, while Dna2 processes only a subset.

Indexed as

Genes, LethalApoptosisCell Cycle ProteinsDNADNA Breaks, Double-StrandedDNA HelicasesDNA RepairFlap EndonucleasesGene DeletionSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTelomeraseCell Cycle ProteinsDNADNA2 protein, S cerevisiaeDNA HelicasesFlap EndonucleasesOkazaki fragmentsPIF1 protein, S cerevisiaeRAD27 protein, S cerevisiaerad9 proteinSaccharomyces cerevisiae ProteinsTelomerase

Identifiers

PMID21508669
PMCPMC3127164
OpenAlexW2014720202

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.