Journal
SCIENCE
Volume 353, Issue 6297, Pages 394-399Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaf4777
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Funding
- March of Dimes [1-FY14-300]
- NIH [GM59083, GM79097, GM118188]
- Research Grants Council of Hong Kong [AoE/M-05/12]
- Grants-in-Aid for Scientific Research [16H05123] Funding Source: KAKEN
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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.
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