Docking of axonal mitochondria by syntaphilin controls their mobility and affects short-term facilitation

作者：Kang, Jian Sheng; Tian, Jin Hua; Pan, Ping Yue; Zald, Philip; Li, Cuiling; Deng, Chuxia; Sheng, Zu Hang^*

来源：Cell, 2008, 132(1): 137-148.

DOI：10.1016/j.cell.2007.11.024

Proper distribution of mitochondria within axons and at synapses is critical for neuronal function. While one-third of axonal mitochondria are mobile, a large proportion remains in a stationary phase. However, the mechanisms controlling mitochondrial docking within axons remain elusive. Here, we report a role for axon-targeted syntaphilin (SNPH) in mitochondrial docking through its interaction with microtubules. Axonal mitochondria that contain exogenously or endogenously expressed SNPH lose mobility. Deletion of the mouse snph gene results in a substantially higher proportion of axonal mitochondria in the mobile state and reduces the density of mitochondria in axons. The snph mutant neurons exhibit enhanced short-term facilitation during prolonged stimulation, probably by affecting calcium signaling at presynaptic boutons. This phenotype is fully rescued by reintroducing the snph gene into the mutant neurons. These findings demonstrate a molecular mechanism for controlling mitochondrial docking in axons that has a physiological impact on synaptic function.

• 出版日期2008-1-11
• 单位上海交通大学