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Role of activation of PIP5Kγ661 by AP-2 complex in synaptic vesicle endocytosis.
- Source :
- EMBO Journal; 2/14/2007, Vol. 26 Issue 4, p1105-1116, 12p
- Publication Year :
- 2007
-
Abstract
- Synaptic vesicles (SVs) are retrieved by clathrin-mediated endocytosis at the nerve terminals. Phosphatidylinositol 4,5-bisphosphate [PI(4,5)P<subscript>2</subscript>] 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<subscript>2</subscript> remain unclear. We demonstrate here that AP-2 complex directly interacts with phosphatidylinositol 4-phosphate 5-kinase γ661 (PIP5Kγ661), the major PI(4,5)P<subscript>2</subscript>-producing enzyme in the brain. The β2 subunit of AP-2 was found to bind to the C-terminal tail of PIP5Kγ661 and cause PIP5Kγ661 activation. The interaction is regulated by PIP5Kγ661 dephosphorylation, which is triggered by depolarization in mouse hippocampal neurons. Finally, overexpression of the PIP5Kγ661 C-terminal region in hippocampal neurons suppresses depolarization-dependent SV endocytosis. These findings provide evidence for the molecular mechanism through which PIP5Kγ661 locally generates PI(4,5)P<subscript>2</subscript> in hippocampal neurons and suggest a model in which the interaction trigger SV endocytosis. [ABSTRACT FROM AUTHOR]
- Subjects :
- ENDOCYTOSIS
PHOSPHOINOSITIDES
ENZYMES
NEURONS
ABSORPTION (Physiology)
Subjects
Details
- Language :
- English
- ISSN :
- 02614189
- Volume :
- 26
- Issue :
- 4
- Database :
- Complementary Index
- Journal :
- EMBO Journal
- Publication Type :
- Academic Journal
- Accession number :
- 24099526
- Full Text :
- https://doi.org/10.1038/sj.emboj.7601573