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Publication : Phosphatidylserine is critical for vesicle fission during clathrin-mediated endocytosis.

First Author  Varga K Year  2020
Journal  J Neurochem Volume  152
Issue  1 Pages  48-60
PubMed ID  31587282 Mgi Jnum  J:282871
Mgi Id  MGI:6383251 Doi  10.1111/jnc.14886
Citation  Varga K, et al. (2020) Phosphatidylserine is critical for vesicle fission during clathrin-mediated endocytosis. J Neurochem 152(1):48-60
abstractText  Phosphatidylserine (PS), a negatively charged phospholipid present predominantly at the inner leaflet of the plasma membrane, has been widely implicated in many cellular processes including membrane trafficking. Along this line, PS has been demonstrated to be important for endocytosis, however, the involved mechanisms remain uncertain. By monitoring clathrin-mediated endocytosis (CME) of single vesicles in mouse chromaffin cells using cell-attached capacitance measurements that offer millisecond time resolution, we demonstrate in the present study that the fission-pore duration is reduced by PS addition, indicating a stimulatory role of PS in regulating the dynamics of vesicle fission during CME. Furthermore, our results show that the PS-mediated effect on the fission-pore duration is Ca(2+) -dependent and abolished in the absence of synaptotagmin 1 (Syt1), implying that Syt1 is necessary for the stimulatory role of PS in vesicle fission during CME. Consistently, a Syt1 mutant with a defective PS-Syt1 interaction increases the fission-pore duration. Taken together, our study suggests that PS-Syt1 interaction may be critical in regulating fission dynamics during CME.
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