ZFIN ID: ZDB-PUB-131024-22
Female and male gamete mitochondria are distinct and complementary in transcription, structure, and genome function
de Paula, W.B., Agip, A.N., Missirlis, F., Ashworth, R., Vizcay-Barrena, G., Lucas, C.H., and Allen, J.F.
Date: 2013
Source: Genome biology and evolution   5(10): 1969-1977 (Journal)
Registered Authors: Ashworth, Rachel
Keywords: mitochondrial DNA, maternal inheritance, Drosophilia melanogaster, Danio rerio, reactive oxygen species, aging
MeSH Terms:
  • Adenosine Triphosphate/biosynthesis
  • Aging/genetics
  • Animals
  • Biological Evolution*
  • DNA, Mitochondrial/genetics*
  • Electron Transport/genetics
  • Female
  • Free Radicals/metabolism
  • Germ Cells/metabolism
  • Male
  • Mitochondria/genetics
  • Mitochondria/metabolism
  • Oocytes/metabolism*
  • Oxygen/metabolism
  • Spermatozoa/metabolism*
  • Transcription, Genetic*
  • Zebrafish/metabolism
PubMed: 24068653 Full text @ Genome Biol. Evol.
ABSTRACT

Respiratory electron transport in mitochondria is coupled to ATP synthesis while generating mutagenic oxygen free radicals. Mitochondrial DNA mutation then accumulates with age, and may set a limit to the lifespan of individual, multicellular organisms. Why is this mutation not inherited? Here we demonstrate that female gametes—oocytes—have unusually small and simple mitochondria that are suppressed for DNA transcription, electron transport, and free radical production. By contrast, male gametes—sperm—and somatic cells of both sexes transcribe mitochondrial genes for respiratory electron carriers and produce oxygen free radicals. This germ-line division between mitochondria of sperm and egg is observed in both the vinegar fruitfly and the zebrafish—species spanning a major evolutionary divide within the animal kingdom. We interpret these findings as an evidence that oocyte mitochondria serve primarily as genetic templates, giving rise, irreversibly and in each new generation, to the familiar energy-transducing mitochondria of somatic cells and male gametes. Suppressed mitochondrial metabolism in the female germ line may therefore constitute a mechanism for increasing the fidelity of mitochondrial DNA inheritance.

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