Phosphoinositides play key regulatory roles in vesicular transport pathways in eukaryotic cells. Clathrin-mediated membrane trafficking has been shown to require phosphoinositides, but little is known about the enzyme(s) responsible for their formation. Here we report that clathrin functions as an adaptor for the class II PI 3-kinase C2alpha (PI3K-C2alpha), binding to its N-terminal region and stimulating its catalytic activity, especially toward phosphorylated inositide substrates. Further, we show that endogenous PI3K-C2alpha is localized in coated pits and that exogenous expression affects clathrin-mediated endocytosis and sorting in the trans-Golgi network. These findings provide a mechanistic basis for localized inositide generation at sites of clathrin-coated bud formation, which, with recruitment of inositide binding proteins and subsequent synaptojanin-mediated phosphoinositide hydrolysis, may regulate coated vesicle formation and uncoating.

Download full-text PDF

Source
http://dx.doi.org/10.1016/s1097-2765(01)00191-5DOI Listing

Publication Analysis

Top Keywords

3-kinase c2alpha
8
clathrin-mediated membrane
8
membrane trafficking
8
class phosphoinositide
4
phosphoinositide 3-kinase
4
c2alpha activated
4
activated clathrin
4
clathrin regulates
4
regulates clathrin-mediated
4
trafficking phosphoinositides
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!