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A more recent version of this article appeared on December 1, 2004
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Submitted on July 9, 2004
Revised on September 24, 2004
Accepted on September 27, 2004
*Vita-Salute University, Dipartimento di Biotecnologie, and San Raffaele Scientific Institute, 20132 Milan, Italy; European Neuroscience Institute Goettingen, 37073 Goettingen, Germany; Department of Pharmacology, University of Milan, 20133 Milan, Italy
Monitoring Editor: Randy Schekman
Enlargeosomes, a new type of widely expressed cytoplasmic vesicles, undergo tetanus toxin-insensitive exocytosis in response to [Ca2+]i rises. Cell biology of enlargeosomes is still largely unknown. By combining immunocytochemistry (marker: desmoyokin-Ahnak, d/A) to capacitance electrophysiology in the enlargeosome-rich, neurosecretion-defective clone PC12-27, we show that the two responses, cell surface enlargement and d/A surface appearance, occur with similar kinetics and in the same low µM [Ca2+]i range, no matter whether induced by photolysis of the caged Ca2+ compound, NP-EGTA, or by the Ca2+ ionophore, ionomycin. Thus, enlargeosomes appear to account, at least in large part, for the exocytic processes triggered by the two stimulations; the enlargeosome membranes are resistant to nonionic detergents but distinct from other resistant membranes, rich in caveolin, Thy1 and/or flotillin1; cell cholesterol depletion, which affects many membrane fusions, neither disrupts enlargeosomes nor affects their regulated exocytosis; the postexocytic cell surface decline is [Ca2+]i-dependent; exocytized d/A-rich membranes are endocytized and trafficked along an intracellular pathway by nonacidic organelles, distinct from classical endosomes and lysosomes. Our data define specific aspects of enlargeosomes and suggest their participation, in addition to cell differentiation and repair, for which evidence already exists, to other physiological and pathological processes.
Corresponding author.
E-mail: meldolesi.jacopo{at}hsr.it
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