Fiche publication
Date publication
février 2013
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BADER Marie-France
,
Dr GASMAN Stéphane
Tous les auteurs :
Ory S, Ceridono M, Momboisse F, Houy S, Chasserot-Golaz S, Heintz D, Calco V, Haeberle AM, Espinoza FA, Sims PJ, Bailly Y, Bader MF, Gasman S
Lien Pubmed
Résumé
Calcium-regulated exocytosis in neuroendocrine cells and neurons is accompanied by the redistribution of phosphatidylserine (PS) to the extracellular space, leading to a disruption of plasma membrane asymmetry. How and why outward translocation of PS occurs during secretion are currently unknown. Immunogold labeling on plasma membrane sheets coupled with hierarchical clustering analysis demonstrate that PS translocation occurs at the vicinity of the secretory granule fusion sites. We found that altering the function of the phospholipid scramblase-1 (PLSCR-1) by expressing a PLSCR-1 calcium-insensitive mutant or by using chromaffin cells from PLSCR-1(-)/(-) mice prevents outward translocation of PS in cells stimulated for exocytosis. Remarkably, whereas transmitter release was not affected, secretory granule membrane recapture after exocytosis was impaired, indicating that PLSCR-1 is required for compensatory endocytosis but not for exocytosis. Our results provide the first evidence for a role of specific lipid reorganization and calcium-dependent PLSCR-1 activity in neuroendocrine compensatory endocytosis.
Référence
J Neurosci. 2013 Feb 20;33(8):3545-56
