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PMID: 24561832 Published · ppublish English Journal Article Research Support, N.I.H., Intramural

Post-fusion structural changes and their roles in exocytosis and endocytosis of dense-core vesicles.

Nature communications ·Vol. 5 ·2014-00-00 ·Pages 3356

Chiang HC, Shin W, Zhao WD, Hamid E, Sheng J, Baydyuk M, Wen PJ, Jin A, Momboisse F, Wu LG

Abstract

Vesicle fusion with the plasma membrane generates an Ω-shaped membrane profile. Its pore is thought to dilate until flattening (full-collapse), followed by classical endocytosis to retrieve vesicles. Alternatively, the pore may close (kiss-and-run), but the triggering mechanisms and its endocytic roles remain poorly understood. Here, using confocal and stimulated emission depletion microscopy imaging of dense-core vesicles, we find that fusion-generated Ω-profiles may enlarge or shrink while maintaining vesicular membrane proteins. Closure of fusion-generated Ω-profiles, which produces various sizes of vesicles, is the dominant mechanism mediating rapid and slow endocytosis within ~1-30 s. Strong calcium influx triggers dynamin-mediated closure. Weak calcium influx does not promote closure, but facilitates the merging of Ω-profiles with the plasma membrane via shrinking rather than full-collapse. These results establish a model, termed Ω-exo-endocytosis, in which the fusion-generated Ω-profile may shrink to merge with the plasma membrane, change in size or change in size then close in response to calcium, which is the main mechanism to retrieve dense-core vesicles.

MeSH Terms
Animals Cattle Cell Membrane/metabolism Cells, Cultured Endocytosis/physiology Exocytosis/physiology Membrane Fusion/physiology Microscopy, Confocal Secretory Vesicles/chemistry,metabolism
Authors & Affiliations
10 authors, click to expand affiliations / ORCID
Chiang Hsueh-Cheng
1] National Institute of Neurological Disorders and Stroke, 35 Convent Drive, Building 35, Room 2B-1012, Bethesda, Maryland 20892, USA [2].
Shin Wonchul
1] National Institute of Neurological Disorders and Stroke, 35 Convent Drive, Building 35, Room 2B-1012, Bethesda, Maryland 20892, USA [2].
Zhao Wei-Dong
National Institute of Neurological Disorders and Stroke, 35 Convent Drive, Building 35, Room 2B-1012, Bethesda, Maryland 20892, USA.
Hamid Edaeni
National Institute of Neurological Disorders and Stroke, 35 Convent Drive, Building 35, Room 2B-1012, Bethesda, Maryland 20892, USA.
Sheng Jiansong
National Institute of Neurological Disorders and Stroke, 35 Convent Drive, Building 35, Room 2B-1012, Bethesda, Maryland 20892, USA.
Baydyuk Maryna
National Institute of Neurological Disorders and Stroke, 35 Convent Drive, Building 35, Room 2B-1012, Bethesda, Maryland 20892, USA.
Wen Peter J
National Institute of Neurological Disorders and Stroke, 35 Convent Drive, Building 35, Room 2B-1012, Bethesda, Maryland 20892, USA.
Jin Albert
National Institute of Biomedical Imaging and Bioengineering (NIBIB), Bethesda, Maryland 20892, USA.
Momboisse Fanny
1] National Institute of Neurological Disorders and Stroke, 35 Convent Drive, Building 35, Room 2B-1012, Bethesda, Maryland 20892, USA [2].
Wu Ling-Gang
National Institute of Neurological Disorders and Stroke, 35 Convent Drive, Building 35, Room 2B-1012, Bethesda, Maryland 20892, USA.
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Article Info
Journal
Nature communications
Abbr.
Nat Commun
ISSN
2041-1723
Published
2014-00-00
Pages
3356
Language
English
Region
England
NLM ID
101528555
PMCID
PMC4267856
Subset
IM
Grants
Intramural NIH HHS · ZIA NS003009-10 · United States
Intramural NIH HHS · ZIA NS003105-05 · United States
Corrections
ErratumIn
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