Mitochondrial endonuclease G mediates breakdown of paternal mitochondria upon fertilization

+ See all authors and affiliations

Science  22 Jul 2016:
Vol. 353, Issue 6297, pp. 394-399
DOI: 10.1126/science.aaf4777

You are currently viewing the abstract.

View Full Text

Eliminating paternal mitochondria

During fertilization, the oocyte and sperm each bring their mitochondria to the union. Shortly afterward, the paternal mitochondria are degraded, and only the maternal mitochondria are conveyed to the progeny. Zhou et al. observed that the integrity of the inner membrane of paternal mitochondria is compromised, which apparently marks them for degradation (see the Perspective by van der Bliek). Autophagy commences by mitochondrial endonuclease G relocating from the intermembrane space into the matrix and subsequently degrading the paternal mitochondrial DNA. Any delay in this process increases embryonic lethality.

Science, this issue p. 394; see also p. 351


Mitochondria are inherited maternally in most animals, but the mechanisms of selective paternal mitochondrial elimination (PME) are unknown. While examining fertilization in Caenorhabditis elegans, we observed that paternal mitochondria rapidly lose their inner membrane integrity. CPS-6, a mitochondrial endonuclease G, serves as a paternal mitochondrial factor that is critical for PME. We found that CPS-6 relocates from the intermembrane space of paternal mitochondria to the matrix after fertilization to degrade mitochondrial DNA. It acts with maternal autophagy and proteasome machineries to promote PME. Loss of cps-6 delays breakdown of mitochondrial inner membranes, autophagosome enclosure of paternal mitochondria, and PME. Delayed removal of paternal mitochondria causes increased embryonic lethality, demonstrating that PME is important for normal animal development. Thus, CPS-6 functions as a paternal mitochondrial degradation factor during animal development.

View Full Text