Cells can regulate the release of membrane proteins from recycling endosomes, thus adjusting the flux of proteins through the transcytotic pathway according to need. This regulation, the mechanism of which is uncertain, allows recycling endosomes to play an important part in adjusting the concentration of specific plasma membrane proteins. Fat cells and muscle cells, for example, contain large intracellular pools of the glucose transporters that are responsible for the uptake of glucose across the plasma membrane. These membrane transport proteins are stored in specialized recycling endosomes until the hormone insulin stimulates the cell to increase its rate of glucose uptake. In response to the insulin signal, transport vesicles rapidly bud from the recycling endosome and deliver large numbers of glucose transporters to the plasma membrane, thereby greatly increasing the rate of glucose uptake into the cell (Figure 13–59). Similarly, kidney cells regulate the insertion of aquaporins and V-ATPase into the plasma membrane to increase water and acid excretion, respectively, both in response to hormones.
Phagocytosis is a special form of endocytosis in which a cell uses large endocytic vesicles called phagosomes to ingest large particles such as microorganisms and dead cells. Phagocytosis is distinct, both in purpose and mechanism, from macropinocytosis, which we discussed earlier. In protozoa, phagocytosis is a form of feeding: large particles taken up into phagosomes end up in lysosomes, and the products of the subsequent digestive processes pass into the cytosol to be used as food. However, few cells in multicellular organisms are able to ingest such large particles efficiently. In the gut of animals, for example, extracellular processes break down food particles, and cells import the small products of hydrolysis.
Figure 13–57 Conserved mechanism in multivesicular body formation and virus budding. In the two topologically equivalent processes indicated by the arrows, escrT complexes (not shown) shape membranes into buds that bulge away from the cytosol.
Figure 13–58 Possible fates for transmembrane receptor proteins that have been endocytosed. Three pathways from the early endosomal compartment in an epithelial cell are shown. retrieved receptors are returned (1) to the same plasma membrane domain from which they came (recycling) or (2) via a recycling endosome to a different domain of the plasma membrane (transcytosis). (3) receptors that are not specifically retrieved from early or recycling endosomes follow the pathway from the endosomal compartment to lysosomes, where they are degraded (degradation). If the ligand that is endocytosed with its receptor stays bound to the receptor in the acidic environment of the endosome, it shares the same fate as the receptor; otherwise, it is delivered to lysosomes. recycling endosomes are a way-station on the transcytotic pathway. In the transcytosis example shown here, an antibody fc receptor on a gut epithelial cell binds antibody and is endocytosed, eventually carrying the antibody to the basolateral plasma membrane. The receptor is called an fc receptor because it binds the fc part of the antibody (discussed in chapter 24).
Figure 13–59 Storage of plasma membrane proteins in recycling endosomes. recycling endosomes can serve as an intracellular storage site for specialized plasma membrane proteins that can be mobilized when needed. In the example shown, insulin binding to the insulin receptor triggers an intracellular signaling pathway that causes the rapid insertion of glucose transporters into the plasma membrane of a fat or muscle cell, greatly increasing its glucose intake.