Ca2+ Triggers a Novel Clathrin‐Independent but Actin‐Dependent Fast Endocytosis in Pancreatic Beta Cells

Z He, J Fan, L Kang, J Lu, Y Xue, P Xu, T Xu, L Chen - Traffic, 2008 - Wiley Online Library
Z He, J Fan, L Kang, J Lu, Y Xue, P Xu, T Xu, L Chen
Traffic, 2008Wiley Online Library
The existence of clathrin‐independent recycling of secretory vesicles has been
controversial. By combining patch‐clamp capacitance recording, optical methods and
specific molecular interventions, we dissect two types of mechanistically different
endocytosis in pancreatic β cells, both of which require GTP and dynamin. The fast one is a
novel clathrin‐independent but actin‐dependent endocytosis that is triggered by high
cytoplasmic Ca2+ concentration ([Ca2+] i). Large fluorescent dextran (10 nm in diameter) …
The existence of clathrin‐independent recycling of secretory vesicles has been controversial. By combining patch‐clamp capacitance recording, optical methods and specific molecular interventions, we dissect two types of mechanistically different endocytosis in pancreatic β cells, both of which require GTP and dynamin. The fast one is a novel clathrin‐independent but actin‐dependent endocytosis that is triggered by high cytoplasmic Ca2+ concentration ([Ca2+]i). Large fluorescent dextran (10 nm in diameter) was able to be internalized by this pathway, indicating that it was not likely to be ‘kiss and run’. The slow endocytosis is a clathrin‐dependent process in which actin plays a complementary role. For the first time, we show that the rate constants for both types of endocytosis exhibit supralinear dependence on increase in [Ca2+]i. Compared with the slow endocytosis, higher [Ca2+]i level was required to fully accelerate the fast one, indicative of distinct Ca2+ sensors for different endocytosis. In the end, we show that physiologically relevant stimulation induces clathrin‐independent endocytosis in intact β cells, implying that it may contribute to the normal recycling of secretory vesicles in vivo.
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