Journal
MECHANISMS OF EXOCYTOSIS
Volume 1152, Issue -, Pages 43-52Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1749-6632.2008.03989.x
Keywords
exocytosis; lung; alveolus; surfactant; type II cell; pneumocyte; fusion pore; FM 1-43; dark-field microscopy; fluorescence microscopy; calcium; C2 ceramide; phospholipase D; phalloidin; kiss-and-run; actin; actin coating; release; surface tension; air-liquid interface; endocytosis; Lamp3; secretory lysosome
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Funding
- Fonds zur Forderung der Wissenschaftlichen Forschung (FWF) [P15742, P15743]
- Deutsche Forschungsgemeinschaft (DFG) [D1402]
- European Union
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Type H pneumocytes secrete surfactant, a lipoprotein-like substance reducing the surface tension in the lung, by regulated exocytosis of secretory vesicles termed lamellar bodies (LBs). This secretory process is characterized by a protracted postfusion phase in which fusion pores open slowly and may act as mechanical barriers for release. Combining dark-field with fluorescence microscopy, we show in beta-actin green fluorescent protein-transfected pneumocytes that LB fusion with the plasma membrane is followed by actin coating of the fused LB. This is inhibited by cytoplasmic Ca2+ chelation or the phospholipase D inhibitor C2 ceramide. Actin coating occurs by polymerization of actin monomers, as evidenced by staining with Alexa 568 phalloidin. After actin coating of the fused LB, it either shrinks while releasing surfactant (kiss-coat-and-release), remains in this fused state without further action (kiss-coat-and-wait), or is retrieved and pushed forward in the cell on top of an actin tail (kiss-coat-and-run). In the absence of actin coating, no release or run was observed. These data suggest that actin coating creates a force needed for either extrusion of vesicle contents or retrieval and intracellular propulsion.
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