Suehiro Yuji
   Department   School of Medicine, School of Medicine
   Position   Assistant Professor
Article types Original article
Language English
Peer review Peer reviewed
Title Mitochondrial endonuclease G mediates breakdown of paternal mitochondria upon fertilization.
Journal Formal name:Science (New York, N.Y.)
ISSN code:(1095-9203)0036-8075(Linking)
Domestic / ForeginForegin
Volume, Issue, Page 353(6297),pp.394-399
Author and coauthor Zhou Qinghua, Li Haimin, Li Hanzeng, Nakagawa Akihisa, Lin Jason L J, Lee Eui-Seung, Harry Brian L, Skeen-Gaar Riley Robert, Suehiro Yuji, William Donna, Mitani Shohei, Yuan Hanna S, Kang Byung-Ho, Xue Ding
Publication date 2016/07
Summary 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.
DOI 10.1126/science.aaf4777
PMID 27338704