Evidence map›Paper›PMID 21109200›Full record

ArticleCell metabolism2010

The mtDNA mutation spectrum of the progeroid Polg mutator mouse includes abundant control region multimers.

Siôn L Williams, Jia Huang, Yvonne J K Edwards, Rick H Ulloa, Lloye M Dillon, Tomas A Prolla, Jeffery M Vance, Carlos T Moraes, Stephan Züchner

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

71 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
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  5. Ubiquitous Expression ofLife (Basel, Switzerland) · 2025
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  8. Necrosis drives susceptibility toInfection and immunity · 2025
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  9. Necrosis drives susceptibility tobioRxiv : the preprint server for biology · 2024
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  10. Review
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  13. mt-tRNAs in the polymerase gamma mutant heart.The journal of cardiovascular aging · 2023
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

11 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

9 authors at 2 institutions in 1 country.

Siôn L WilliamsDepartment of Neurology, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Jia Huang
Yvonne J K Edwards
Rick H Ulloa
Lloye M Dillon
Tomas A Prolla
Jeffery M Vance
Carlos T Moraes
Stephan Züchner
University of Miami · USUniversity of Wisconsin–Madison · US

Funding

Vitamin D Concentration, Genetic Modifiers, and Parkinson DiseaseP50NS071674 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI VANCE, JEFFERY MARVIN · 2010 to 2015
$10.2M
SETTING THE STAGE FOR REPLACEMENT OF MITOCHONDRIAL GENESR01EY010804 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 1995 to 2025
$9.4M
Mitochondrial Dysfunction in Neurodegeneration and Compensatory ApproachesR01AG036871 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2010 to 2020
$3.3M
Mouse Models with Defective Respiratory Complexes in CNSR01NS041777 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2001 to 2009
$2.4M
OXIDATIVE PHOSPHORYLATION IN CELL GROWTH AND DEATHR01CA085700 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2001 to 2010
$2.2M
The Pathophysiology of CMT2A in Cell and Animal ModelsR01NS052767 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ZUCHNER, STEPHAN · 2006 to 2010
$1.7M
Mouse Models of Mitochondrial EncephalomyopathiesR56NS041777 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2010 to 2010
$445k
NCI NIH HHS CA85700NCI NIH HHS R01 CA085700NEI NIH HHS EY10804NEI NIH HHS R01 EY010804NIA NIH HHS AG036871NIA NIH HHS R01 AG036871NINDS NIH HHS NS053767NINDS NIH HHS P50 NS071674NINDS NIH HHS P50NS071674NINDS NIH HHS R01 NS041777NINDS NIH HHS R01 NS052767NINDS NIH HHS R56 NS041777
6 · The paper itself

Abstract

Polg mtDNA mutator mice are important models for investigating the role of acquired mtDNA mutations in aging. Despite extensive study, there remains little consensus on either the etiology of the progeroid phenotype or the mtDNA mutation spectrum induced by disrupted polymerase-γ function. To investigate the latter, we have developed a novel, pragmatic approach we term "Mito-seq," applying next-generation sequencing to enriched, native mtDNA. Regardless of detection parameters we observed an increase of at least two orders of magnitude in the number of mtDNA single nucleotide variants in Polg mutator mice compared to controls. We found no evidence for the accumulation of canonical mtDNA deletions but multimers of the mtDNA control region were identified in brain and heart. These control region multimers (CRMs) contained heterogeneous breakpoints and formed species that excluded the majority of mtDNA genes. CRMs demonstrate that polymerase-γ 3'-5' exonuclease activity is required for preserving mtDNA integrity.

Indexed as

AgingAnimalsBase SequenceBlotting, SouthernDNA-Directed DNA PolymeraseDNA, MitochondrialDNA Polymerase gammaLocus Control RegionMiceMice, Inbred C57BLMice, Mutant StrainsMolecular Sequence DataPolymerase Chain ReactionPolymorphism, Single NucleotideProgeriaSequence Analysis, DNADNA-Directed DNA PolymeraseDNA, MitochondrialDNA Polymerase gammaPolg protein, mouse

Identifiers

PMID21109200
PMCPMC3175596
OpenAlexW1967253002

What OpenQuestion holds

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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.