Evidence map›Paper›PMID 22214610›Full record

ArticleGenetics2012

Mitochondrial genome maintenance: roles for nuclear nonhomologous end-joining proteins in Saccharomyces cerevisiae.

Lidza Kalifa, Daniel F Quintana, Laura K Schiraldi, Naina Phadnis, Garry L Coles, Rey A Sia, Elaine A Sia

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Manipulating and elucidating mitochondrial gene expression with engineered proteins.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Review
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  18. Minimizing the damage: repair pathways keep mitochondrial DNA intact.Nature reviews. Molecular cell biology · 2012
    Review
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

7 authors at 2 institutions in 1 country.

Lidza KalifaDepartment of Biology, University of Rochester, Rochester, New York 14627, USA.
Daniel F Quintana
Laura K Schiraldi
Naina Phadnis
Garry L Coles
Rey A Sia
Elaine A Sia
University of Rochester · USSUNY Brockport · US

Funding

Genes Involved in Recovery from UV-Induced Mitochondrial DNA DamageF31GM078700 · NIGMS · UNIVERSITY OF ROCHESTER · PI KALIFA, LIDZA · 2007 to 2010
$160k
NIGMS NIH HHS F31 GM078700
6 · The paper itself

Abstract

Mitochondrial DNA (mtDNA) deletions are associated with sporadic and inherited diseases and age-associated neurodegenerative disorders. Approximately 85% of mtDNA deletions identified in humans are flanked by short directly repeated sequences; however, mechanisms by which these deletions arise are unknown. A limitation in deciphering these mechanisms is the essential nature of the mitochondrial genome in most living cells. One exception is budding yeast, which are facultative anaerobes and one of the few organisms for which directed mtDNA manipulation is possible. Using this model system, we have developed a system to simultaneously monitor spontaneous direct-repeat-mediated deletions (DRMDs) in the nuclear and mitochondrial genomes. In addition, the mitochondrial DRMD reporter contains a unique KpnI restriction endonuclease recognition site that is not present in otherwise wild-type (WT) mtDNA. We have expressed KpnI fused to a mitochondrial localization signal to induce a specific mitochondrial double-strand break (mtDSB). Here we report that loss of the MRX (Mre11p, Rad50p, Xrs2p) and Ku70/80 (Ku70p, Ku80p) complexes significantly impacts the rate of spontaneous deletion events in mtDNA, and these proteins contribute to the repair of induced mtDSBs. Furthermore, our data support homologous recombination (HR) as the predominant pathway by which mtDNA deletions arise in yeast, and suggest that the MRX and Ku70/80 complexes are partially redundant in mitochondria.

Indexed as

Antigens, NuclearCell NucleusDeoxyribonucleases, Type II Site-SpecificDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA End-Joining RepairDNA, MitochondrialDNA RepairEndodeoxyribonucleasesExodeoxyribonucleasesGene OrderGenome, MitochondrialKu AutoantigenMitochondriaModels, GeneticMutation RateAntigens, NuclearDeoxyribonucleases, Type II Site-SpecificDNA-Binding ProteinsDNA, MitochondrialEndodeoxyribonucleasesExodeoxyribonucleasesGGTACC-specific type II deoxyribonucleasesKu AutoantigenMRE11 protein, S cerevisiaeNuclear ProteinsRAD50 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsXrcc6 protein, humanXRS2 protein, S cerevisiae

Identifiers

PMID22214610
PMCPMC3296257
OpenAlexW2129308451

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.