Endocytosis is a type of active transport that moves particles, such as large molecules, parts of cells, and even whole cells, into a cell. There are different endocytosis variations, but all share a common characteristic: the cell's plasma membrane invaginates, forming a pocket around the target particle. The pocket pinches off, resulting in the particle containing itself in a newly created intracellular vesicle formed from the plasma membrane.
Phagocytosis (the condition of “cell eating”) is the process by which a cell takes in large particles, such as other cells or relatively large particles. For example, when microorganisms invade the human body, a type of white blood cell, a neutrophil, will remove the invaders through this process, surrounding and engulfing the microorganism, which the neutrophil then destroys (Figure).
In preparation for phagocytosis, a portion of the plasma membrane's inward-facing surface becomes coated with the protein clathrin, which stabilizes this membrane's section. The membrane's coated portion then extends from the cell's body and surrounds the particle, eventually enclosing it. Once the vesicle containing the particle is enclosed within the cell, the clathrin disengages from the membrane and the vesicle merges with a lysosome for breaking down the material in the newly formed compartment (endosome). When accessible nutrients from the vesicular contents' degradation have been extracted, the newly formed endosome merges with the plasma membrane and releases its contents into the extracellular fluid. The endosomal membrane again becomes part of the plasma membrane.
A variation of endocytosis is pinocytosis. This literally means “cell drinking”. Discovered by Warren Lewis in 1929, this American embryologist and cell biologist described a process whereby he assumed that the cell was purposefully taking in extracellular fluid. In reality, this is a process that takes in molecules, including water, which the cell needs from the extracellular fluid. Pinocytosis results in a much smaller vesicle than does phagocytosis, and the vesicle does not need to merge with a lysosome (Figure).
A variation of pinocytosis is potocytosis. This process uses a coating protein, caveolin, on the plasma membrane's cytoplasmic side, which performs a similar function to clathrin. The cavities in the plasma membrane that form the vacuoles have membrane receptors and lipid rafts in addition to caveolin. The vacuoles or vesicles formed in caveolae (singular caveola) are smaller than those in pinocytosis. Potocytosis brings small molecules into the cell and transports them through the cell for their release on the other side, a process we call transcytosis.
A targeted variation of endocytosis employs receptor proteins in the plasma membrane that have a specific binding affinity for certain substances (Figure).
In receptor-mediated endocytosis, as in phagocytosis, clathrin attaches to the plasma membrane's cytoplasmic side. If a compound's uptake is dependent on receptor-mediated endocytosis and the process is ineffective, the material will not be removed from the tissue fluids or blood. Instead, it will stay in those fluids and increase in concentration. The failure of receptor-mediated endocytosis causes some human diseases. For example, receptor mediated endocytosis removes low density lipoprotein or LDL (or "bad" cholesterol) from the blood. In the human genetic disease familial hypercholesterolemia, the LDL receptors are defective or missing entirely. People with this condition have life-threatening levels of cholesterol in their blood, because their cells cannot clear LDL particles.
Although receptor-mediated endocytosis is designed to bring specific substances that are normally in the extracellular fluid into the cell, other substances may gain entry into the cell at the same site. Flu viruses, diphtheria, and cholera toxin all have sites that cross-react with normal receptor-binding sites and gain entry into cells.
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See receptor-mediated endocytosis in action, and click on different parts for a focused animation.