Evidence map›Paper›PMID 18562670›Full record

ArticleGenetics2008

A genetic screen for increased loss of heterozygosity in Saccharomyces cerevisiae.

Marguerite P Andersen, Zara W Nelson, Elizabeth D Hetrick, Daniel E Gottschling

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

68 citing papers in PubMed, 94 citations in OpenAlex.

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  16. rDNA array length is a major determinant of replicative lifespan in budding yeast.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  18. Review
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8 more citing papers are in PubMed but not listed here.

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.

Marguerite P AndersenDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
Zara W Nelson
Elizabeth D Hetrick
Daniel E Gottschling
Fred Hutch Cancer Center · US

Funding

Mechanism of increase genomic instability in aging yeastR01AG023779 · NIA · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PARKHURST, SUSAN M · 2004 to 2019
$4.2M
Seattle Cancer and Aging ProgramP20CA103728 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI RABINOVITCH, PETER S · 2003 to 2007
$3.4M
Dissecting the mechanism of increased genomic instability in aging yeastR37AG023779 · NIA · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GOTTSCHLING, DANIEL E. · 2010 to 2015
$2.9M
NCI NIH HHS CA-103728NCI NIH HHS P20 CA103728NIA NIH HHS AG-023779NIA NIH HHS R01 AG023779NIA NIH HHS R37 AG023779
6 · The paper itself

Abstract

Loss of heterozygosity (LOH) can be a driving force in the evolution of mitotic/somatic diploid cells, and cellular changes that increase the rate of LOH have been proposed to facilitate this process. In the yeast Saccharomyces cerevisiae, spontaneous LOH occurs by a number of mechanisms including chromosome loss and reciprocal and nonreciprocal recombination. We performed a screen in diploid yeast to identify mutants with increased rates of LOH using the collection of homozygous deletion alleles of nonessential genes. Increased LOH was quantified at three loci (MET15, SAM2, and MAT) on three different chromosomes, and the LOH events were analyzed as to whether they were reciprocal or nonreciprocal in nature. Nonreciprocal LOH was further characterized as chromosome loss or truncation, a local mutational event (gene conversion or point mutation), or break-induced replication (BIR). The 61 mutants identified could be divided into several groups, including ones that had locus-specific effects. Mutations in genes involved in DNA replication and chromatin assembly led to LOH predominantly via reciprocal recombination. In contrast, nonreciprocal LOH events with increased chromosome loss largely resulted from mutations in genes implicated in kinetochore function, sister chromatid cohesion, or relatively late steps of DNA recombination. Mutants of genes normally involved in early steps of DNA damage repair and signaling produced nonreciprocal LOH without an increased proportion of chromosome loss. Altogether, this study defines a genetic landscape for the basis of increased LOH and the processes by which it occurs.

Indexed as

AllelesChromatin Assembly and DisassemblyChromosomes, FungalCysteine SynthaseDNA Breaks, Double-StrandedDNA ReplicationGene DeletionGenes, FungalGenetic MarkersGenomic InstabilityLoss of HeterozygosityMultienzyme ComplexesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCysteine SynthaseGenetic MarkersMET17 protein, S cerevisiaeMultienzyme ComplexesSaccharomyces cerevisiae Proteins

Identifiers

PMID18562670
PMCPMC2475725
OpenAlexW2139316770

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.