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| Research article summary (published 19 Aug 2009): |
Synaptotagmin-mediated bending of the target membrane is a critical step in Ca(2+)-regulated fusion.
Full Abstract
Decades ago it was proposed that exocytosis involves invagination of the target membrane, resulting in a highly localized site of contact between the bilayers destined to fuse. The vesicle protein synaptotagmin-I (syt) bends membranes in response to Ca(2+), but whether this drives localized invagination of the target membrane to accelerate fusion has not been determined. Previous studies relied on reconstituted vesicles that were already highly curved and used mutations in syt that were not selective for membrane-bending activity. Here, we directly address this question by utilizing vesicles with different degrees of curvature. A tubulation-defective syt mutant was able to promote fusion between highly curved SNARE-bearing liposomes but exhibited a marked loss of activity when the membranes were relatively flat. Moreover, bending of flat membranes by adding an N-BAR domain rescued the function of the tubulation-deficient syt mutant. Hence, syt-mediated membrane bending is a critical step in membrane fusion.
Author information
Author/s: Hui, Enfu (E); Johnson, Colin P (CP); Yao, Jun (J); Dunning, F Mark (FM); Chapman, Edwin R (ER);
Affiliation: Howard Hughes Medical Institute, USA.
Grants: MH61876 (Agency:NIMH NIH HHS) ; (Agency:Howard Hughes Medical Institute)
Journal and publication information
Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Journal: Cell (Cell), published in United States. (Language: eng)
Reference: 2009-Aug; vol 138 (issue 4) : pp 709-21
Dates: Created 2009/08/25; Completed 2009/09/23; Revised 2009/10/07;
PMID: 19703397, status: MEDLINE (last retrieval date: 10/8/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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