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Measuring Single-Cell Mitochondrial DNA Copy Number and Heteroplasmy Using Digital Droplet Polymerase Chain Reaction
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Published on: July 12, 2022

Mitochondrial DNA copy number and function decrease with age in the short-lived fish Nothobranchius furzeri.

Nils Hartmann1, Kathrin Reichwald, Ilka Wittig

  • 1Department of Molecular Genetics, Leibniz Institute for Age Research-Fritz Lipmann Institute (FLI), Beutenbergstrasse 11, Jena, Germany. hartmann@fli-leibniz.de

Aging Cell
|June 1, 2011
PubMed
Summary
This summary is machine-generated.

Aging in the short-lived annual fish (Nothobranchius furzeri) involves decreased mitochondrial DNA (mtDNA) copy number and impaired mitochondrial function, despite no age-related mtDNA deletions. This fish model offers insights into aging processes.

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A Protocol for Laboratory Housing of Turquoise Killifish (Nothobranchius furzeri)

Published on: April 11, 2018

Area of Science:

  • Gerontology
  • Mitochondrial Biology
  • Comparative Physiology

Background:

  • The annual fish Nothobranchius furzeri is a vertebrate model with the shortest known lifespan, exhibiting aging signs.
  • It serves as an ideal model to study aging and lifespan determination due to its rapid aging process.

Purpose of the Study:

  • To investigate the association between aging and mitochondrial DNA (mtDNA) alterations in Nothobranchius furzeri.
  • To assess age-related changes in mitochondrial function in this model organism.

Main Methods:

  • Sequencing of the complete mitochondrial genome of N. furzeri.
  • Quantification of mtDNA copy number across various tissues (skeletal muscle, brain, liver, skin, dorsal fin).
  • Analysis of gene expression for mitochondrial biogenesis (Pgc-1α) and mtDNA binding factors (Tfam, mtSsbp).
  • Assessment of mitochondrial respiratory chain complex content and respiratory function in skeletal muscle.

Main Results:

  • No age-related large-scale mtDNA deletions were detected.
  • A significant decrease in mtDNA copy number was observed with age in multiple tissues.
  • Downregulation of Pgc-1α, Tfam, and mtSsbp gene expression was noted in aging fish.
  • Reduced content of respiratory chain complexes III and IV, and impaired mitochondrial respiration (ADP-stimulated and succinate-dependent) were found in older fish.

Conclusions:

  • Aging in N. furzeri is characterized by a decline in mtDNA copy number and impaired mitochondrial function.
  • Downregulation of key mtDNA-associated genes accompanies aging in this model.
  • Despite its short lifespan, N. furzeri provides valuable insights into the molecular mechanisms of aging.