Mode Of Endocytosis Research Articles

Food uptake and the fine structure of the dinophytePaulsenella sp. an ectoparasite of marine diatoms

Motile dinospores ofPaulsenella attach to a host diatom frustule, form a feeding tube, drive it between epi- and hypocingulum, pierce the host plasmalemma and suck up host cytoplasm gradually. This mode of endocytosis (“myzocytosis”) implies that the host plasmalemma is not ingested and that the host cytoplasm within the food vacuole is bounded only by the vacuolar membrane. The feeding tube is formed by the emergence of a preformed “microtubular basket” consisting of plates of microtubules. At its entrance into the cell body the feeding tube channel is surrounded by an electron-dense ring. Similar “sphincters” enclose the two exits through which the two flagella emerge. These sphincters are composed of microfibrils which reveal a cross striation when the fixative does not contain calcium ions. The flagellar bases as well as the internal part of the feeding tube are surrounded by a common cavity which is in open connection also with the ampullae of the pusule. The light and electron microscopical observations do not support the assumption that food uptake is driven by a flow of the membrane of the feeding tube channel caused by an interaction with the microtubular basket (as postulated for food uptake inSuctoria) but rather by an hydrostatic gradient which might be caused by rhythmical ion pumping and be based on the existence of the common cavity and the sphincters. Myzocytosis is inhibited by cytochalasin B.—The fine structure of dinospores and trophonts, especially with respect to the cell covering, the amphiesma, and the en- and excystment, is described.

Modes of endocytosis of latex particles in sinusoidal endothelial and kupffer cells of normal and perfused rat liver

The endocytosis of latex particles (0.33, 0.46 and 0.80 μm in diameter) in the sinusoidal endothelial and Kupffer cells of the rat liver was studied electron microscopically. When the liver was perfused with serum-free oxygenated Krebs Ringer bicarbonate, latex particles of all three sizes were taken up by the endothelial cells. After a 10-min perfusion, particles were incorporated by the luminal cell surface of the perikarya or of the thick portion of the endothelial cells. A large patch of bristle coat was surrounding the ingested particle. The number of ingested particles in the endothelial cells, however, was much less than in the Kupffer cells. In in vivo experiments, no endocytosis of the latex particles was observed in the endothelial cells. In the Kupffer cells, particles were engulfed by the ruffled membranes or sank into the cytoplasm without a large patch of the bristle coat both in the perfusion system and in vivo. These observations show that at least 0.80 μm latex particles are taken up by the bristle-coated membranes in the sinusoidal endothelial cells of the perfused liver. The endocytic mechanism for latex particles in the endothelial cells is different from that of the Kupffer cells.

A comparative study of the effects of polyamino acids and dextran derivatives on pinocytosis in the rat yolk sac and the rat peritoneal macrophage

Poly- l-lysine, poly- l-α-ornithine, poly- l-glutamic acid, dextran, DEAE-dextran and dextran sulphate all fail to affect greatly the rate of pinocytic uptake of 125I-labelled polyvinylpyrrolidone by 17.5-day rat visceral yolk sac or rat peritoneal macrophages cultured in vitro. It is concluded that these agents do not much affect the rate of pinocytic ingestion of liquid. Polycations accelerate the accumulation of colloidal 198Au in both systems, and this is ascribed to the formation of substrate · modifier complexes which either adsorb to plasma membrane, and thus gain rapid entry, or initiate another mode of endocytosis. Pinocytic uptake of formaldehyde-denatured 125I-labelled bovine serum albumin was accelerated by poly- l-lysine and poly- l-ga-ornithine in the macrophage, buth inhibited in the yolk sac.