中文摘要：

ubiquitin ligase Parkin 和 autophagic 改编者蛋白质 p62 被知道在控制 mitochondrial autophagy (mitophagy ) 的一条普通小径工作。然而，支持那 p62 被 ubiquitinated 蛋白质直接招募的证据仍然保持未经决定。这里，我们证明那个 mitochondrial 分裂因素(Mff ) 与 Parkin 联系，羰基氰化物 m-chlorophenyl hydrazone 处理显著地与 Mff 增加 Parkin 的亲密关系。在到动摇线粒体的招募以后， Parkin 调停在离氨酸 251 点的 Mff 的 poly-ubiquitination。由精氨酸(K251R ) 的离氨酸 251 的代替完全废除 Mff 的刺激 Parkin 的 ubiquitination。随后， ubiquitinated Mff 与 p62 支持它的协会。Mff 大美人防碍 p62 translocation 到损坏线粒体。仅仅 Mff WT 的 re-transfection，然而并非 K251R 异种，救这显型。而且， Mff 的损失导致 Parkin translocation 和损坏线粒体的最后的清理的失败。因此，我们的数据在 Mff， p62，和线粒体的选择 autophagy 之中揭示功能的连接，它在 neurodegeneration 疾病的致病被含有。

英文摘要：

The ubiquitin ligase Parkin and autophagic adapter protein p62 are known to function in a common pathway controlling mitochondrial autophagy （mitophagy）. However, the evidence supporting that p62 is directly recruited by ubiquitinated proteins remains undetermined. Here, we demonstrate that mitochondrial fission factor （Mff） associates with Parkin and carbonyl cyanide m-chlorophenyl hydrazone treatment significantly increases the affinity of Parkin with Mff. After recruitment to depo- larized mitochondria, Parkin mediates poly-ubiquitination of Mff at lysine 251. Replacement of lysine 251 by arginine （K251R） totally abrogates Parkin-stimulated ubiquitination of Mff. Subsequently, the ubiquitinated Mff promotes its association with p62. Mff knockout interferes with p62 translocation to damaged mitochondria. Only re-transfection of Mff WT, but not K251R mutant, rescues this pheno- type. Furthermore, loss of Mff results in failure of Parkin translocation and final clearance of damaged mitochondria. Thus, our data reveal functional links among Mff, p62, and the selective autophagy of mitochondria, which are implicated in the pathogenesis of neurodegeneration diseases.