What is Endocytosis?

Endocytosis brings material in: the plasma membrane invaginates around it and pinches off a vesicle, which generally fuses with a lysosome. Phagocytosis engulfs particles (a bacterium, a dead cell); pinocytosis takes in droplets of fluid; receptor-mediated endocytosis concentrates a particular molecule (cholesterol-carrying particles, iron-carrying transferrin) on receptors in coated pits before taking it in. Exocytosis adds membrane to the cell surface and endocytosis removes it; in a secreting cell the two balance so that the surface stays constant while whole areas of membrane cycle through it every hour.

Receptor-mediated endocytosis concentrates a ligand bound to surface receptors into clathrin-coated pits, which pinch off (the GTPase dynamin constricts the neck) as vesicles of about $100\,\mathrm{nm}$ — a thousand per minute in a fibroblast, turning over the whole surface membrane in an hour. The vesicles fuse into early endosomes, whose lumen is acidified to pH 6 by a proton pump; most ligands release their receptors there, the receptors return to the surface in recycling vesicles, and the ligand travels on as the endosome matures into a late endosome (pH 5.5) and fuses with a lysosome: a compartment at pH 4.5–5 holding some sixty hydrolases — proteases, nucleases, lipases, glycosidases — active only at that pH, so that a leak into the neutral cytosol does little harm. The lysosome also digests the cell’s own material delivered by autophagy: a double membrane grows around a portion of cytoplasm or a worn-out organelle, closes into an autophagosome, and fuses with the lysosome; the products are returned to the cytosol. Autophagy is induced by starvation (it recycles a cell’s own substance for energy) and clears aggregates and damaged mitochondria; its failure is implicated in neurodegeneration.