Evidence map›Paper›PMID 21745495›Full record

ArticleMechanisms of ageing and development

The role of DMQ(9) in the long-lived mutant clk-1.

Yu-Ying Yang, Valeria Vasta, Sihoun Hahn, Jon A Gangoiti, Elyce Opheim, Margaret M Sedensky, Phil G Morgan

Open access · greenAbstract read
In one paragraph

Article in Mechanisms of ageing and development. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. A novelMolecular genetics and metabolism reports · 2022
    Article
  3. Article
  4. Review
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  6. Article
  7. Metabolic Targets of Coenzyme Q10 in Mitochondria.Antioxidants (Basel, Switzerland) · 2021
    Review
  8. Article
  9. Article
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  11. Article
  12. Article
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  15. Review
  16. Article
  17. Article
  18. Article
  19. Molecular genetics of ubiquinone biosynthesis in animals.Critical reviews in biochemistry and molecular biology
    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 3 institutions in 1 country.

Yu-Ying YangDepartment of Genetics, Case Western Reserve University, Cleveland, OH, United States. yyy4@uw.edu
Valeria Vasta
Sihoun Hahn
Jon A Gangoiti
Elyce Opheim
Margaret M Sedensky
Phil G Morgan
Seattle Children's Hospital · USUniversity of Washington · USUniversity of California, San Diego · US

Funding

MITOCHONDRIAL EFFECTS ON SENSITIVITY TO ANESTHETICSR01GM058881 · NIGMS · SEATTLE CHILDREN'S HOSPITAL · PI SEDENSKY, MARGARET MARY · 1999 to 2009
$3.9M
Interaction of ubiquinone &complex I control longevityR01AG026073 · NIA · SEATTLE CHILDREN'S HOSPITAL · PI MORGAN, PHILIP G · 2005 to 2009
$1.5M
NIA NIH HHS AG026073NIA NIH HHS R01 AG026073NIGMS NIH HHS 3R01GM58881-12S1NIGMS NIH HHS GM5881NIGMS NIH HHS R01 GM058881
6 · The paper itself

Abstract

introductionUbiquinone (UQ) is a redox active lipid that transfers electrons from complex I or II to complex III in the electron transport chain (ETC). The long-lived Caenorhabditis elegans mutant clk-1 is unable to synthesize its native ubiquinone, and accumulates high amounts of its precursor, 5-demethoxyubiquinone-9 (DMQ(9)). In clk-1, complexes I-III activity is inhibited while complexes II-III activity is normal. We asked whether the complexes I-III defect in clk-1 was caused by: (1) a defect in the ETC; (2) an inhibitory effect of DMQ(9); or (3) a decreased amount of ubiquinone.

methodsWe extracted the endogenous quinones from wildtype (N2) and clk-1 mitochondria, replenished them with exogenous ubiquinones, and measured ETC activities.

resultsReplenishment of extracted mutant and wildtype mitochondria resulted in equal enzymatic activities for complexes I-III and II-III ETC assays. Blue native gels showed that supercomplex formation was indistinguishable between clk-1 and N2. The addition of a pentane extract from clk-1 mitochondria containing DMQ(9) to wildtype mitochondria specifically inhibited complexes I-III activity. UQ in clk-1 mitochondria was oxidized compared to N2. DISCUSSION: Our results show that no measurable intrinsic ETC defect exists in clk-1 mitochondria. The data indicate that DMQ(9) specifically inhibits electron transfer from complex I to ubiquinone.

Indexed as

MutationAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsElectron Transport Chain Complex ProteinsLongevityMitochondriaUbiquinone5-demethoxyubiquinone-9Caenorhabditis elegans ProteinsCLK-1 protein, C elegansElectron Transport Chain Complex ProteinsUbiquinone

Identifiers

PMID21745495
PMCPMC3156029
OpenAlexW2056306864

What OpenQuestion holds

Textmetadata
LicenceTDM
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.