Document Detail


Myosin Va transports dense core secretory vesicles in pancreatic MIN6 beta-cells.
MedLine Citation:
PMID:  15788565     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The role of unconventional myosins in neuroendocrine cells is not fully understood, with involvement suggested in the movement of both secretory vesicles and mitochondria. Here, we demonstrate colocalization of myosin Va (MyoVa) with insulin in pancreatic beta-cells and show that MyoVa copurifies with insulin in density gradients and with the vesicle marker phogrin-enhanced green fluorescent protein upon fluorescence-activated sorting of vesicles. By contrast, MyoVa immunoreactivity was poorly colocalized with mitochondrial or other markers. Demonstrating an important role for MyoVa in the recruitment of secretory vesicles to the cell surface, a reduction of MyoVa protein levels achieved by RNA interference caused a significant decrease in glucose- or depolarization-stimulated insulin secretion. Similarly, expression of the dominant-negative-acting globular tail domain of MyoVa decreased by approximately 50% the number of vesicles docked at the plasma membrane and by 87% the number of depolarization-stimulated exocytotic events detected by total internal reflection fluorescence microscopy. We conclude that MyoVa-driven movements of vesicles along the cortical actin network are essential for the terminal stages of regulated exocytosis in beta-cells.
Authors:
Aniko Varadi; Takashi Tsuboi; Guy A Rutter
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-03-23
Journal Detail:
Title:  Molecular biology of the cell     Volume:  16     ISSN:  1059-1524     ISO Abbreviation:  Mol. Biol. Cell     Publication Date:  2005 Jun 
Date Detail:
Created Date:  2005-06-03     Completed Date:  2005-11-21     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  9201390     Medline TA:  Mol Biol Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2670-80     Citation Subset:  IM    
Affiliation:
Henry Wellcome Laboratories for Integrated Cell Signalling, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom.
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MeSH Terms
Descriptor/Qualifier:
Animals
Biological Markers / metabolism
Biological Transport*
Cell Culture Techniques
Cell Line, Tumor
Cell Membrane / metabolism
Centrifugation, Density Gradient
Exocytosis
Glucose / pharmacology
Green Fluorescent Proteins / metabolism
Humans
Immunohistochemistry
Insulin / isolation & purification,  metabolism
Islets of Langerhans / metabolism*
Membrane Proteins / metabolism
Mice
Microscopy, Interference
Mutation
Myosin Heavy Chains / chemistry,  genetics,  isolation & purification,  metabolism*
Myosin Type V / chemistry,  genetics,  isolation & purification,  metabolism*
Pancreas / cytology*
Protein Structure, Tertiary
Protein Tyrosine Phosphatases / metabolism
RNA Interference
Receptor-Like Protein Tyrosine Phosphatases, Class 8
Secretory Vesicles / metabolism*
Grant Support
ID/Acronym/Agency:
//Wellcome Trust
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Insulin; 0/Membrane Proteins; 0/Myo5a protein, mouse; 0/Myosin Heavy Chains; 147336-22-9/Green Fluorescent Proteins; 148971-15-7/MYO5A protein, human; 50-99-7/Glucose; EC 3.1.3.48/PTPRN2 protein, human; EC 3.1.3.48/Protein Tyrosine Phosphatases; EC 3.1.3.48/Receptor-Like Protein Tyrosine Phosphatases, Class 8; EC 3.6.1.-/Myosin Type V
Comments/Corrections

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