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An integrase of endogenous retrovirus is involved in maternal mitochondrial DNA inheritance of the mouse

Kenji Hayashida1, Katsuhisa Omagari, Jun-Ichi Masuda

  • 1Second Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki 852-8501, Japan.

Biochemical and Biophysical Research Communications
|December 7, 2007
PubMed

Insights

Maternal mitochondrial DNA (mtDNA) inheritance is established by eliminating sperm mtDNA. Researchers identified an endogenous retroviral integrase fragment (Eri15) that complexes with Spag1 proteins to destroy sperm mtDNA.

Area of Science:

  • Reproductive Biology
  • Genetics
  • Molecular Biology

Background:

  • Maternal inheritance of mitochondrial DNA (mtDNA) in animals relies on selective elimination of paternal sperm mtDNA.
  • Previous work identified Spag1 isoform 1 as a sperm mitochondria-specific translocator and suggested egg factors involved in sperm mtDNA elimination.

Purpose of the Study:

  • To identify the egg's elimination factors responsible for sperm mtDNA degradation.
  • To elucidate the molecular mechanism underlying maternal mtDNA inheritance.

Main Methods:

  • Recombinant Spag1 isoform 1 protein was used in pull-down assays with ovary cytosol.
  • Mass spectrometry was employed to identify proteins interacting with Spag1.
  • Native polyacrylamide gel electrophoresis (PAGE) was used to analyze protein complexes.

Main Results:

  • An endogenous retroviral integrase fragment (Eri15) was identified as a novel factor interacting with Spag1.
  • Eri15 formed a large complex (approx. 500kDa) with Spag1 isoform 2 or 3 in ovary cytosol.
  • Evidence suggests Eri15 is transported into sperm mitochondria via Spag1 isoforms, leading to sperm mtDNA destruction.

Conclusions:

  • The study identifies Eri15 as a key component of the sperm mtDNA elimination system.
  • Spag1 isoforms mediate the transport and function of Eri15, ensuring maternal mtDNA inheritance.
  • This discovery provides critical insights into the molecular mechanisms controlling mitochondrial DNA inheritance.

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