Abstract:
:Disruption of the presynaptically enriched polyphosphoinositide phosphatase synaptojanin 1 leads to an increase of clathrin-coated intermediates and of polymerized actin at endocytic zones of nerve terminals. These changes correlate with elevated levels of PI(4,5)P(2) in neurons. We report that phosphatidylinositol phosphate kinase type Igamma (PIPKIgamma), a major brain PI(4)P 5-kinase, is concentrated at synapses. Synaptojanin 1 and PIPKIgamma antagonize each other in the recruitment of clathrin coats to lipid membranes. Like synaptojanin 1 and other proteins involved in endocytosis, PIPKIgamma undergoes stimulation-dependent dephosphorylation. These results implicate PIPKIgamma in the synthesis of a PI(4,5)P(2) pool that acts as a positive regulator of clathrin coat recruitment and actin function at the synapse.
journal_name
Neuronjournal_title
Neuronauthors
Wenk MR,Pellegrini L,Klenchin VA,Di Paolo G,Chang S,Daniell L,Arioka M,Martin TF,De Camilli Pdoi
10.1016/s0896-6273(01)00456-1subject
Has Abstractpub_date
2001-10-11 00:00:00pages
79-88issue
1eissn
0896-6273issn
1097-4199pii
S0896-6273(01)00456-1journal_volume
32pub_type
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