Role of activation of PIP5Kγ661 by AP-2 complex in synaptic vesicle endocytosis

被引:64
作者
Nakano-Kobayashi, Akiko
Yamazaki, Masakazu
Unoki, Takamitsu
Hongu, Tsunaki
Murata, Chie
Taguchi, Ryo
Katada, Toshiaki
Frohman, Michael A.
Yokozeki, Takeaki
Kanaho, Yasunori
机构
[1] Univ Tsukuba, Grad Sch Comprehens Human Sci, Dept Physiol Chem, Tsukuba, Ibaraki 3050006, Japan
[2] Univ Tsukuba, Inst Basic Med Sci, Tsukuba, Ibaraki 3050006, Japan
[3] Univ Tokyo, Grad Sch Pharmaceut Sci, Dept Physiol Chem, Tokyo, Japan
[4] Univ Tokyo, Grad Sch Med, Dept Metabolome, Tokyo, Japan
[5] SUNY Stony Brook, Ctr Dev Genet, New York, NY USA
[6] SUNY Stony Brook, Dept Pharmacol, New York, NY USA
关键词
AP-2; complex; phosphatidylinositol; 4-phosphate; 5-kinase; PI(4,5)P-2; synaptic vesicle endocytosis;
D O I
10.1038/sj.emboj.7601573
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Synaptic vesicles (SVs) are retrieved by clathrin-mediated endocytosis at the nerve terminals. Phosphatidylinositol 4,5-bisphosphate [PI( 4,5) P-2] drives this event by recruiting the components of the endocytic machinery. However, the molecular mechanisms that result in local generation of PI( 4,5) P-2 remain unclear. We demonstrate here that AP-2 complex directly interacts with phosphatidylinositol 4-phosphate 5-kinase gamma 661 (PIP5Kc661), the major PI(4,5) P-2-producing enzyme in the brain. The beta 2 subunit of AP-2 was found to bind to the C-terminal tail of PIP5Kc661 and cause PIP5Kc661 activation. The interaction is regulated by PIP5Kc661 dephosphorylation, which is triggered by depolarization in mouse hippocampal neurons. Finally, overexpression of the PIP5Kc661 C-terminal region in hippocampal neurons suppresses depolarization-dependent SV endocytosis. These findings provide evidence for the molecular mechanism through which PIP5Kc661 locally generates PI( 4,5) P-2 in hippocampal neurons and suggest a model in which the interaction trigger SV endocytosis.
引用
收藏
页码:1105 / 1116
页数:12
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