Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2014) 35 S8.2 | DOI: 10.1530/endoabs.35.S8.2


Leibniz Institut für Molekulare Pharmakolgie, Berlin, Germany.


Phosphoinositides (PIs) serve crucial roles in cell physiology ranging from cell signalling to membrane traffic. Among the seven eukaryotic PIs the best studied species is phosphatidylinositol (4,5)-bisphosphate (PI(4,5)P2), which is concentrated at the plasma membrane where among many other functions it is required for the nucleation of endocytic clathrin-coated pits (CCPs). No PI other than PI(4,5)P2 has been implicated in clathrin-mediated endocytosis (CME), whereas the subsequent endosomal stages of the endocytic pathway are dominated by PI 3-phosphates. How PI conversion from PI(4,5)P2-positive endocytic intermediates to PI 3-phosphate (PI(3)P)-containing endosomes and, conversely, from PI(3)P-positive endosomes to plasma membrane PI(4,5)P2 is achieved is unclear.

In my talk I will summarize our recent findings regarding the mechanisms of PI conversion between the plasma membrane and endosomes. We recently demonstrated that formation of phosphatidylinositol-3, 4-bisphosphate (PI(3,4)P2) by class II phosphatidylinositol 3-kinase C2α (PI3K C2α) spatiotemporally controls CME by regulating maturation of late-stage CCPs before fission. Timed formation of PI(3,4)P2 by PI3K C2α is required for selective enrichment of the BAR domain protein SNX9 at late-stage endocytic intermediates. Combined mathematical modelling, super-resolution imaging, and genetic manipulations provide a mechanistic framework for PI conversion from PI(4,5)P2 to PI(3,4)P2 en route to endosomes. Furthermore, I will discuss our most recent data on the role of PI conversion in endosomal homeostasis and recycling to the plasma membrane.

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