Rapid depletion of ESCRT protein Vps4 underlies injury-induced autophagic impediment and Wallerian degeneration
Rapid depletion of ESCRT protein Vps4 underlies injury-induced autophagic impediment and Wallerian degeneration
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ESCRT 蛋白 Vps4 的快速消耗是损伤引起的自噬障碍和华勒变性的基础
DOI：
10.1126/sciadv.aav4971
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发表时间：
2019-02
期刊：
影响因子：
13.6
通讯作者：
Fang Yanshan
中科院分区：
文献类型：
--
作者：
Wang Haiqiong;Wang Xuejie;Zhang Kai;Wang Qingyao;Cao Xu;Wang Zhao;Zhang Shuang;Li Ang;Liu Kai;Fang Yanshan
ESCRT复合蛋白Vps4在神经损伤时迅速耗竭，导致自噬障碍和轴突退化。受损的轴突会经历一个受控制的自我破坏过程，被称为沃勒变性。然而，潜在的机制……
The ESCRT complex protein Vps4 is rapidly depleted upon nerve injury, causing autophagic impediment and axonal degeneration. Injured axons undergo a controlled, self-destruction process, known as Wallerian degeneration. However, the underlying mechanism remains elusive. Using the Drosophila wing nerve as a model, we identify the ESCRT component Vps4 as a previously unidentified essential gene for axonal integrity. Up-regulation of Vps4 remarkably delays degeneration of injured axons. We further reveal that Vps4 is required and sufficient to promote autophagic flux in axons and mammalian cells. Moreover, using both in vitro and in vivo models, we show that the function of Vps4 in maintaining axonal autophagy and suppressing Wallerian degeneration is conserved in mammals. Last, we uncover that Vps4 protein is rapidly depleted in injured mouse axons, which may underlie the injury-induced autophagic impediment and the subsequent axonal degeneration. Together, Vps4 and ESCRT may represent a novel signal transduction mechanism in axon injury and Wallerian degeneration.
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影响因子：
5.7
作者：
S. Tooze;G. Schiavo
通讯作者：
S. Tooze;G. Schiavo
神经元自噬和轴突变性
影响因子：
8
作者：
Wang Yu;Song Mingxue;Song Fuyong
通讯作者：
Song Fuyong
影响因子：
21.3
作者：
Wakatsuki, Shuji;Saitoh, Fuminori;Araki, Toshiyuki
通讯作者：
Araki, Toshiyuki
影响因子：
16.2
作者：
Essuman K;Summers DW;Sasaki Y;Mao X;DiAntonio A;Milbrandt J
通讯作者：
Milbrandt J
影响因子：
9.2
作者：
Fang, Yanshan;Soares, Lorena;Teng, Xiuyin;Geary, Melissa;Bonini, Nancy M
通讯作者：
Bonini, Nancy M