Mitochondrial endonuclease G mediates breakdown of paternal mitochondria upon fertilization.
Mitochondrial endonuclease G mediates breakdown of paternal mitochondria upon fertilization.
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DOI：
10.1126/science.aaf4777
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发表时间：
2016-07-22
期刊：
影响因子：
--
通讯作者：
Xue D
中科院分区：
文献类型：
--
作者：
Zhou Q;Li H;Li H;Nakagawa A;Lin JL;Lee ES;Harry BL;Skeen-Gaar RR;Suehiro Y;William D;Mitani S;Yuan HS;Kang BH;Xue D
线粒体在大多数动物中是母系遗传的，但选择性父系线粒体消除（PME）的机制尚不清楚。在研究C. elegans，我们观察到父亲线粒体迅速失去其内膜完整性。CPS-6是一种线粒体核酸内切酶G，作为父系线粒体因子，对PME至关重要。CPS-6核酸内切酶在受精后从父本线粒体的膜间隙重新定位到基质以降解线粒体DNA。它与母体自噬和蛋白酶体机制一起促进PME。cps-6的缺失延迟了线粒体内膜的破裂、父本线粒体的自噬体外壳和PME。延迟去除父本线粒体导致胚胎死亡率增加，表明PME对正常动物发育很重要。因此，CPS-6在动物发育过程中作为父系线粒体降解因子发挥作用。
Mitochondria are inherited maternally in most animals, but the mechanisms of selective paternal mitochondrial elimination (PME) are unknown. While examining fertilization in C. elegans, we observe 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. The CPS-6 endonuclease relocates from the intermembrane space of paternal mitochondria to the matrix following 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.