Information

Why is phagocytosis not included as a type of receptor-mediated endocytosis?


A common classification of endocytotic processes groups them into Phagocytosis, Pinocytosis, and receptor-mediated endocytosis (1) & (2). But Phagocytosis involves the use of specific receptors like opsonin receptors, toll-like receptors, etc (3). Why then does this classification still hold?

(1) https://courses.lumenlearning.com/boundless-biology/chapter/bulk-transport/

(2) Essentials of Medical Physiology 6th edition by K. Sembulingam and Preya Sembulingam (page 34)

(3) Histology_A text_and_an_atlas_with_correlated_cell_and_molecular_biology 6th Edition (page 32)


Moving Components Through the Cell

3 Receptor-Mediated Endocytosis

RME [11,12] is also known as clathrin-dependent endocytosis because of involvement of the membrane-associated protein clathrin in forming membrane vesicles that become internalized into the cell. Clathrin plays a major role in formation of clathrin-coated pits and coated vesicles. Since clathrin was first isolated and named by Barbara Pearse in 1975 [13] , it has become clear that clathrin and other coat proteins play essential roles in cell biology. Clathrin is an essential component in building small vesicles for uptake (endocytosis) and export (exocytosis) of many molecules. While the methods of membrane transport, discussed in Chapter 19 , involved small solutes, RME is the primary mechanism for the specific internalization of most macromolecules by eukaryotic cells.

RME begins with an external ligand binding to a specific receptor that spans the plasma membrane ( Fig. 17.3 , [14,15] ). Examples of these ligands include hormones, growth factors, enzymes, serum proteins, low-density lipoprotein (LDL) (with attached cholesterol), transferrin (with attached iron), antibodies, some viruses, and even bacterial toxins. After receptor binding, the complex diffuses laterally in the plasma membrane until it encounters a specialized patch of membrane called a coated pit. The receptor–ligand complexes accumulate in these patches as do other proteins including clathrin, adaptor protein, and dynamin. Since coated pits occupy about 20% of the plasma membrane surface area, they are not minor membrane features. The collection of these proteins starts to curve the adjacent section of the membrane that eventually pinches off to form an internalized coated vesicle. Clathrin and dynamin then recycle back to the plasma membrane, leaving an uncoated vesicle that is free to fuse with an early endosome. After the early endosomes mature into late endosomes, they then go to the lysosome for digestion. RME is a very fast process. Invagination and vesicle formation take about 1 min. One single cultured fibloblast cell can produce 2500 coated pits per minute.

Figure 17.3 . Receptor mediated endocytosis (also known as clathrin-dependent endocytosis).

Reference Grant BD, Sato M. http://www.wormbook.org/chapters/www_intracellulartrafficking/intracellulartrafficking.html 2006.

One example of RME has received a great deal of attention because of its essential role in human health, namely maintaining the proper level of cholesterol in the body. Malfunctions in the RME process for uptake of cholesterol-carrying LDL (see Chapter 14 ) leads to hypercholesterolemia and cardiovascular disease [11,16] . RME and its role in cholesterol metabolism was discovered by Michael Brown and Joseph Goldstein of The University of Texas Health Science Center in Dallas (now the UT Southwestern Medical Center), who received the 1985 Nobel Prize in Physiology and Medicine for their iconic work.


Receptor Mediated Endocytosis—Internalization steps

Receptor mediated endocytosis is a process by which cells internalize molecules or viruses. As its name implies, it depends on the interaction of that molecule with a specific binding protein in the cell membrane called a receptor. The following case will illustrate why you need to know about this clinically important cellular event. It is illustrated in the cartoon and electron micrographs in the side bar.

Study this unit and then return to the case with answers for Mr. Murphy.

Define major internalization routes:

The above figure diagrams the major internalization events. In the two views on the right, receptors are not needed for internalization. During phagocytosis, cells may simply internalize particles or cells, like bacteria (cell eating). In the second, called pinocytosis, cells internalize soluble material (cell drinking). In both types of internalization, the cells extend processes and bring cells or soluble material into the cell in a vacuole. In the presentation on lysosomes , we learned that the vacuole formed in the cell by phagocytosis or pinocytosis often became a lysosome after hydrolases were brought to it and the pH was adjusted. The vacuoles formed are called phagosomes or macropinosomes

Endosomes are formed by receptor-mediated endocytosis. In this case, cells bring in proteins and other types of ligands attached to the plasma membrane via receptors. The process depends first on specific binding to the receptor, which is a subject worthy of a lecture in itself. This figure shows this process as "coated pit endocytosis". The coated pit is a specialized region of the membrane that is coated with clathrin (for stability, to aid the transport process). The coated pit forms a coated vesicle and then loses its clathrin coat. It then joins with other coated pits to form a receptosome.

What types of ligands enter by receptor mediated endocytosis?

Toxins and lectins

  • Diptheria Toxin
  • Pseudomonas toxin
  • Cholera toxin
  • Ricin
  • Concanavalin A
  • Rous sarcoma virus
  • Semliki forest virus
  • Vesicular stomatitis virus
  • Adenovirus

Serum transport proteins and antibodies

  • Transferrin
  • Low density lipoprotein
  • Transcobalamin
  • Yolk proteins
  • IgE
  • Polymeric IgA
  • Maternal IgG
  • IgG, via Fc receptors

Hormones and Growth Factors

  • Insulin
  • Epidermal Growth Factor
  • Growth Hormone
  • Thyroid stimulating hormone
  • Nerve Growth Factor
  • Calcitonin
  • Glucagon
  • Prolactin
  • Luteinizing Hormone
  • Thyroid hormone
  • Platelet Derived Growth Factor
  • Interferon
  • Catecholamines

How does the process work? An overview:

Receptors are brought to the plasma membrane by vesicles from the trans region of the Golgi complex . Review the definition of transmembrane proteins. Where and how are these receptor proteins inserted into the membrane? How does the Golgi complex maintain the fluidity of the plasma membrane, the receptors can move laterally in the membrane and collect in the specialized regions called clathrin coated pits.

When the ligand binds to its specific receptor, the ligand-receptor complex accumulates in the coated pits. In many cells, these pits and complexes begin to concentrate in one area of a cell. Cytochemically, this appears as patches of label on the cell surface (patching) Eventually, the patches coalesce to form a cap at one pole of the cell (capping) Not all cells form caps, but most do form patches. Why would this process be an advantage for the cells? Imagine the large amounts of extracellular fluid that would be taken up if the cells endocytosed the ligand receptor complex all over its surface. Thus, the pre-concentration process minimizes the amount of fluid that is taken up in the vesicle. Below is a micrograph showing the patching of receptors at one pole of the cell (Arrows, black labeling).

Effect of temperature on the process.

This table was taken from Endocytosis, Edited by Ira Pastan and Mark C. Willingham, Plenum Press, N.Y., 1985

To understand patching and capping, recall the studies of membranes and Membrane fluidity. Receptors are moving in the plane of the membrane as long as the temperature is 37 C. In the presentation on Membrane fluidity, we talked about photobleaching with a laser beam. This allows you to study the lateral diffusion coefficients of the ligand-receptor complexes. Fluorescent molecules signal the site of the complexes and they are bleached after the laser exposure. Then, the photobleaching system measures the speed of the recovery in the bleached area (return of the fluorescence) as the label returns by lateral diffusion.

An example of some measurements for different receptors is found in this table. The objective of the lateral movement is to collect the ligand-receptor complex in the clathrin coated pits. So, some receptors appear to be moving faster than others. One might speculate that this may be related to size of the receptor or the ligand.

Temperature may affect the binding of the ligand (rate) as well as the lateral mobility of the ligand-receptor complex. Some ligands will not bind well at low temperatures. However, others will bind, but not be taken in. This photograph shows the peroxidase (HRP) detection of a ligand that is distributed on the membrane at 4 C. Note the right hand control panel that shows absence of label in the presence of competing unlabeled ligand. Note the presence of the coated pit, even in the control. So, the formation of these is not temperature dependent. However, after warming for a few minutes, the formation of vesicles and endosomes is evident. It is important to note that Receptor mediated endocytosis is much faster than phagocytosis or pinocytosis. If one were to simply have a non-binding ligand present, it might take hours for the ligand to enter via pinocytosis. Thus, this rapid uptake coupled with the absence of label in the presence of competing ligand is a sign that this is receptor mediated.

This figure was taken from Endocytosis, Edited by Ira Pastan and Mark C. Willingham, Plenum Press, N.Y., 1985

Some coated vesicles may be configured with a deep invagination, called a "neck". These were discovered by Willingham and Pastan and can be seen in serial sections as a thin region connection between the outside of the membrane and the vesicle. The vesicle contains labeled ligand attached to receptor. Formation of these necks is definitely temperature dependent as can be seen in the following table.

This figure and Table were taken from Endocytosis, Edited by Ira Pastan and Mark C. Willingham, Plenum Press, N.Y., 1985

Finally, temperature is important to the overall patching and capping process discussed during the lecture on membranes. There we showed that, after they are bound, Membrane Receptors move laterally in the plane and groups of receptor-ligand complexes may actually coalesce in a patch and eventually in a cap. Antibodies are good examples of receptors that react this way. The left hand figure (above) shows what happens if the temperature is 4 C. There is a diffuse labeling. Warming the cells immediately produces patching.

This figure was taken from Endocytosis, Edited by Ira Pastan and Mark C. Willingham, Plenum Press, N.Y., 1985

Formation of Cathrin Coated Pits

Clathrin coats surround the pit as diagrammed in the above cartoon. The assembly of the clathrin molecules on the pit appears to drive the pit to invaginate. This cage-like molecule may help stabilize the vesicle as it buds from the membrane.

Clathrin coated pits may move in the plane of the membrane, however recent studies show that there is an "organized movement" as if the pits are tethered to cytoskeletal elements. The following paper studies coated pits in living cells that were transfected with a plasmid carrying a cDNA for green fluorescent protein (GFP) attached to the light chain of clathrin. Gaidarov I, Santini, F, Warren, RA and Keen, JH Spatial control of coated-pit dynamics in living cells. Nature, Cell Biology 1: 1-7. 1999.

The cells made GFP-clathrin and were able to insert the protein into coated pits. This was tested via antibodies to coated pit proteins as well as studies of the endocytosis of transferrin. When time lapse photography was used to learn if the coated pits moved, they found that the pits appeared and disappeared at intervals. Studies of regional spacing showed that appearance of new pits was often close to sites of old pits, suggesting regional organization. Superimposed images showed a linear pattern as if the pits were organized.

The studies showed that the coated pits were resistent to detergents (Triton-X). And, they were able to show that the retraction of cellular processes that followed triton-X treatment produced linear movement of each coated pit in the plasma membrane as if it was organized by or on cytoskeletal elements. See the paper by this group (above citation) for the photographs and movies of these findings.

Role of beta-Arrestins in guiding receptors to the clathrin-coated pits.

Beta-arrestin forms a complex with Adaptin (AP-2) and clathrin to both guide the receptor into the pit and keep it there.

Can more than one receptor type enter a vesicle?

Supposing a cell is stimulated with two hormones (and it has receptors for both), or a hormone and a growth factor. Do both ligands enter via the same packages, or is there a selection for one particular type of ligand in a coated pit. This is a perfect question for cytochemistry with different types of labels attached to different ligands. For example, one can use colloidal gold, ferritin, peroxidase and detect as many as 2-4 ligands on a given cell.

The following figure shows that multiple ligands can enter the cell in the same coated pit. Furthermore, the vesicles will carry them to the same receptosomes. The photo shows co-detection of ligands as diverse as Epidermal growth factor, vesicular stomatitis virus, or alpha 2 macroglobulin. Labeling molecules (signalling molecules) included gold, peroxidase, ferritin, or the virus itself. This figure was taken from Endocytosis, Edited by Ira Pastan and Mark C. Willingham, Plenum Press, N.Y., 1985


Formation of Endocytic vesicles.

Once the vesicle has formed, the clathrin coat is lost (perhaps via a chaperone protein of the heat shock protein 70 family). The loss of the coat is an energy requiring process. After the coat is lost, the vesicles join with other vesicles to form endosomes or receptosomes. The following electron micrograph shows clathrin coated pits forming a vesicle. It is taking up lipoprotein particles. Note how thick and well defined the clathrin coat is.

This micrograph was taken from Endocytosis, Edited by Ira Pastan and Mark C. Willingham, Plenum Press, N.Y., 1985

Low Density Lipoprotein Receptors are a good example of receptor-mediated endocytosis.

LDL carries cholesterol to the cells and bind specific receptors which undergo receptor mediated endocytosis to provide an important source of cholesterol for all cells. LDL is considered the “bad cholesterol”, only if it fails to get into the cell and ends up in the blood stream. How could that happen? There are clinical conditions in which the LDL receptors are defective. The discovery of this clinically important system resulted in Nobel Prizes for Brown and Goldstein!!

Now, you can solve Mr. Murphy’s case!! The important thing to remember is the type of defect. It is in the LDL receptor! This is often a question on boards and you may have to identify which molecule is defective from a selection, including: AP-2, Adaptin, clathrin, LDL, LDL receptor, Arrestin, etc. So, if you know the function of each of the players, you can answer the Board questions accurately. Go over the process of internalization until you know the steps and each of the molecules involved.

Can You Distinguish profiles showing exocytosis and endocytosis?

Clathrin coated pits serve like a flat "basket", stabilizing the area to be internalized. They are not exclusive to the plasma membrane. However, it is important to be able to distinguish them from exocytosis profiles associated with the plasma membrane which serve as the secretory route for secreted products such as hormones, neurotransmitters, growth factors, etc.


For example, the above electron micrograph is showing the process of exocytosis . The process begins by fusion of the membranes at the peripheral pole of the granule. Then an opening is created which widens to look like an omicron figure. This opening allows the granular material to be released. The membrane is now part of the plasma membrane and any proteins carried with it can be incorporated into the plasma membrane. Note that there is no coating on the membrane. This figure was taken from Alberts et al, Molecular Biology of the Cell, Garland Publishing Third Edition, 1994

Receptor Mediated Endocytosis

In contrast, this micrograph shows a figure which looks something like an omicron, however, this view is showing receptor mediated endocytosis of virus particles. In both cases, the membrane is coated with clathrin and these represent classical receptor mediated endocytosis profiles. Most ligands cannot be visualized by themselves, like a virus particle. Therefore, the cytochemist must attach label to the ligand. Alternatively, the cytochemist could immunocytochemically detect the receptor with antibodies that recognize the extracellular domain. This figure was taken from Endocytosis , Edited by Ira Pastan and Mark C. Willingham, Plenum Press, N.Y., 1985


Continue studies of Receptor Mediated Endocytosis to learn what happens after Internalization!


5.4 Bulk Transport

Diffusion, osmosis, and active transport are used to transport fairly small molecules across plasma cell membranes. However, sometimes large particles, such as macromolecules, parts of cells, or even unicellular microorganisms, can be engulfed by other cells in a process called phagocytosis or “cell eating.” In this form of endocytosis, the cell membrane surrounds the particle, pinches off, and brings the particle into the cell. For example, when bacteria invade the human body, a type of white blood cell called a neutrophil will remove the invaders by this process. Similarly, in pinocytosis or “cell drinking,” the cell takes in droplets of liquid. In receptor-mediated endocytosis, uptake of substances by the cell is targeted to a single type of substance that binds to a specific receptor protein on the external surface of the cell membrane (e.g., hormones and their target cells) before under going endocytosis. Some human diseases, such as familial hypercholesterolemia, are caused by the failure of receptor-mediated endocytosis. Exocytosis is the process of exporting material out of the cell vesicles containing substances fuse with the plasma membrane and the contents are released to the exterior of the cell. The secretion of neurotransmitters at synapses between neurons is an example of exocytosis.

Information presented and the examples highlighted in the section support concepts and learning objectives outlined in Big Idea 2 of the AP ® Biology Curriculum Framework. The learning objectives listed in the Curriculum Framework provide a transparent foundation for the AP ® Biology course, an inquiry-based laboratory experience, instructional activities, and AP ® exam questions. A learning objective merges required content with one or more of the seven science practices.

Big Idea 2 Biological systems utilize free energy and molecular building blocks to grow, to reproduce, and to maintain dynamic homeostasis.
Enduring Understanding 2.B Growth, reproduction and dynamic homeostasis require that cells create and maintain internal environments that are different from their external environments.
Essential Knowledge 2.B.2 Growth and dynamic homeostasis are maintained by the constant movement of molecules across membranes.
Science Practice 1.4 The student can use representations and models to analyze situations or solve problems qualitatively and quantitatively.
Learning Objective 2.12 The student is able to use representations and models to analyze situations or solve problems qualitatively and quantitatively to investigate whether dynamic homeostasis is maintained by the active movement of molecules across membranes.
Big Idea 2 Biological systems utilize free energy and molecular building blocks to grow, to reproduce, and to maintain dynamic homeostasis.
Enduring Understanding 2.D Growth and dynamic homeostasis of a biological system are influenced by changes in the system’s environment.
Essential Knowledge 2.D.4 Plants and animals have a variety of chemical defenses against infections that affect dynamic homeostasis.
Science Practice 1.1 The student can create representations and models of natural or man-made phenomena and systems in the domain.
Science Practice 1.2 The student can describe representations and models of natural or man-made phenomena and systems in the domain.
Learning Objective 2.30 The student can create representations or models to describe nonspecific immune defenses in plants and animals.

Teacher Support

Ask students to consider how large polar molecules required by cells, such as proteins and polysaccharides, can enter cells when they are unable to cross cell membranes. These molecules enter cells through the active transport mechanism of endocytosis. This video on endocytosis and exocytosis can be used to demonstrate this information.

In addition to moving small ions and molecules through the membrane, cells also need to remove and take in larger molecules and particles (see Table 5.2 for examples). Some cells are even capable of engulfing entire unicellular microorganisms. You might have correctly hypothesized that the uptake and release of large particles by the cell requires energy. A large particle, however, cannot pass through the membrane, even with energy supplied by the cell.

Endocytosis

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 variations of endocytosis, but all share a common characteristic: The plasma membrane of the cell invaginates, forming a pocket around the target particle. The pocket pinches off, resulting in the particle being contained in a newly created intracellular vesicle formed from the plasma membrane.

Phagocytosis

Phagocytosis (the condition of “cell eating”) is the process by which large particles, such as cells or relatively large particles, are taken in by a cell. For example, when microorganisms invade the human body, a type of white blood cell called a neutrophil will remove the invaders through this process, surrounding and engulfing the microorganism, which is then destroyed by the neutrophil (Figure 5.21).

In preparation for phagocytosis, a portion of the inward-facing surface of the plasma membrane becomes coated with a protein called clathrin , which stabilizes this section of the membrane. The coated portion of the membrane then extends from the body of the cell 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 the breakdown of the material in the newly formed compartment (endosome). When accessible nutrients from the degradation of the vesicular contents 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.

Science Practice Connection for AP® Courses

Activity

Create a representation/diagram to describe how a neutrophil, a type of human white blood cell, attacks and destroys an invading bacterium. What cellular organelles are involved in this process?

Teacher Support

Student diagrams should show receptors in the neutrophil that bind to the bacteria and the plasma membrane of the neutrophil surrounding the bacteria. The diagram should also show a lysosome merging with vesicle containing the bacteria, and breakdown of the bacteria by the lysosome.

Pinocytosis

A variation of endocytosis is called pinocytosis . This literally means “cell drinking” and was named at a time when the assumption was 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 5.23).

A variation of pinocytosis is called potocytosis . This process uses a coating protein, called caveolin , on the cytoplasmic side of the plasma membrane, 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 is used to bring small molecules into the cell and to transport these molecules through the cell for their release on the other side of the cell, a process called transcytosis.

Receptor-mediated Endocytosis

A targeted variation of endocytosis employs receptor proteins in the plasma membrane that have a specific binding affinity for certain substances (Figure 5.24).

In receptor-mediated endocytosis , as in phagocytosis, clathrin is attached to the cytoplasmic side of the plasma membrane. If uptake of a compound 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. Some human diseases are caused by the failure of receptor-mediated endocytosis. For example, the form of cholesterol termed low-density lipoprotein or LDL (also referred to as “bad” cholesterol) is removed from the blood by receptor-mediated endocytosis. 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 from their blood.

Although receptor-mediated endocytosis is designed to bring specific substances that are normally found 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.

Link to Learning

See receptor-mediated endocytosis in action, and click on different parts for a focused animation.

  1. The bacteria will be destroyed and will not cause any illness.
  2. The bacteria will survive but will not cause illness.
  3. The bacteria will be destroyed, but will still cause illness.
  4. The bacteria will survive and possibly will cause illness.

Exocytosis

The reverse process of moving material into a cell is the process of exocytosis. Exocytosis is the opposite of the processes discussed above in that its purpose is to expel material from the cell into the extracellular fluid. Waste material is enveloped in a membrane and fuses with the interior of the plasma membrane. This fusion opens the membranous envelope on the exterior of the cell, and the waste material is expelled into the extracellular space (Figure 5.25). Other examples of cells releasing molecules via exocytosis include the secretion of proteins of the extracellular matrix and secretion of neurotransmitters into the synaptic cleft by synaptic vesicles.


Difference between Endocytosis and Phagocytosis

Definition

Endocytosis: Endocytosis refers to taking in of matter into a living cell by the forming of a vesicle by the cell membrane.

Phagocytosis: Phagocytosis refers to the taking in of large solid matter into the cell by forming phagosomes.

Correspondence

Endocytosis: Endocytosis is composed of three categories: phagocytosis, pinocytosis and receptor-mediated endocytosis.

Phagocytosis: Phagocytosis is a category of endocytosis.

Material taken up

Endocytosis: During endocytosis, both macromolecules and particles are taken into the cell.

Phagocytosis: During phagocytosis, only particles are taken into the cell.

Conclusion

Endocytosis is the taking in of matter into the cell for various metabolic purposes. It is categorized into three types of mechanisms, based on the distinct types of material taken in. Large solid particles like cell debris, dead cells, and bacteria-like pathogens are taken up by phagocytosis. Phagocytosis is involved in the defense mechanisms of the cell. Fluids and dissolved solutes in it are taken up by pinocytosis. Almost all the cells in the body take in nutrients, ions, and other macromolecules into the cell by pinocytosis. The third and the most specific mechanism of endocytosis is receptor-mediated endocytosis. During receptor-mediated endocytosis, receptors in the plasma membrane identify the macromolecules like cholesterol in the extracellular fluid. However, the main difference between endocytosis and phagocytosis is their correlation of the mechanisms.

Reference:
1. Alberts, Bruce. “Transport into the Cell from the Plasma Membrane: Endocytosis.” Molecular Biology of the Cell. 4th edition. U.S. National Library of Medicine, 01 Jan. 1970. Web. 31 Mar. 2017.
2. Cooper, Geoffrey M. “Endocytosis.” The Cell: A Molecular Approach. 2nd edition. U.S. National Library of Medicine, 01 Jan. 1970. Web. 31 Mar. 2017.

Image Courtesy:
1. “Endocytosis types” By Mariana Ruiz Villarreal LadyofHats – Own work (Public Domain) via Commons Wikimedia
2. “Phagocytosis2” By GrahamColm at English Wikipedia (CC BY-SA 3.0) via Commons Wikimedia

About the Author: Lakna

Lakna, a graduate in Molecular Biology & Biochemistry, is a Molecular Biologist and has a broad and keen interest in the discovery of nature related things


25 Bulk Transport

By the end of this section, you will be able to do the following:

  • Describe endocytosis, including phagocytosis, pinocytosis, and receptor-mediated endocytosis
  • Understand the process of exocytosis

In addition to moving small ions and molecules through the membrane, cells also need to remove and take in larger molecules and particles (see (Figure) for examples). Some cells are even capable of engulfing entire unicellular microorganisms. You might have correctly hypothesized that when a cell uptakes and releases large particles, it requires energy. A large particle, however, cannot pass through the membrane, even with energy that the cell supplies.

Endocytosis

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

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.

Pinocytosis

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.

Receptor-mediated Endocytosis

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.

See receptor-mediated endocytosis in action, and click on different parts for a focused animation.

Exocytosis

The reverse process of moving material into a cell is the process of exocytosis. Exocytosis is the opposite of the processes we discussed above in that its purpose is to expel material from the cell into the extracellular fluid. Waste material is enveloped in a membrane and fuses with the plasma membrane’s interior. This fusion opens the membranous envelope on the cell’s exterior, and the waste material expels into the extracellular space ((Figure)). Other examples of cells releasing molecules via exocytosis include extracellular matrix protein secretion and neurotransmitter secretion into the synaptic cleft by synaptic vesicles.


Methods of Transport, Energy Requirements, and Types of Transported Material
Transport Method Active/Passive Material Transported
Diffusion Passive Small-molecular weight material
Osmosis Passive Water
Facilitated transport/diffusion Passive Sodium, potassium, calcium, glucose
Primary active transport Active Sodium, potassium, calcium
Secondary active transport Active Amino acids, lactose
Phagocytosis Active Large macromolecules, whole cells, or cellular structures
Pinocytosis and potocytosis Active Small molecules (liquids/water)
Receptor-mediated endocytosis Active Large quantities of macromolecules

Section Summary

Active transport methods require directly using ATP to fuel the transport. In a process scientists call phagocytosis, other cells can engulf large particles, such as macromolecules, cell parts, or whole cells. In phagocytosis, a portion of the membrane invaginates and flows around the particle, eventually pinching off and leaving the particle entirely enclosed by a plasma membrane’s envelope. The cell breaks down vesicle contents, with the particles either used as food or dispatched. Pinocytosis is a similar process on a smaller scale. The plasma membrane invaginates and pinches off, producing a small envelope of fluid from outside the cell. Pinocytosis imports substances that the cell needs from the extracellular fluid. The cell expels waste in a similar but reverse manner. It pushes a membranous vacuole to the plasma membrane, allowing the vacuole to fuse with the membrane and incorporate itself into the membrane structure, releasing its contents to the exterior.

Review Questions

What happens to the membrane of a vesicle after exocytosis?

  1. It leaves the cell.
  2. It is disassembled by the cell.
  3. It fuses with and becomes part of the plasma membrane.
  4. It is used again in another exocytosis event.

Which transport mechanism can bring whole cells into a cell?

  1. pinocytosis
  2. phagocytosis
  3. facilitated transport
  4. primary active transport

In what important way does receptor-mediated endocytosis differ from phagocytosis?

  1. It transports only small amounts of fluid.
  2. It does not involve the pinching off of membrane.
  3. It brings in only a specifically targeted substance.
  4. It brings substances into the cell, while phagocytosis removes substances.

Many viruses enter host cells through receptor-mediated endocytosis. What is an advantage of this entry strategy?

  1. The virus directly enters the cytoplasm of the cell.
  2. The virus is protected from recognition by white blood cells.
  3. The virus only enters its target host cell type.
  4. The virus can directly inject its genome into the cell’s nucleus.

Which of the following organelles relies on exocytosis to complete its function?

Imagine a cell can perform exocytosis, but only minimal endocytosis. What would happen to the cell?

  1. The cell would secrete all its intracellular proteins.
  2. The plasma membrane would increase in size over time.
  3. The cell would stop expressing integral receptor proteins in its plasma membrane.
  4. The cell would lyse.

Critical Thinking Questions

Why is it important that there are different types of proteins in plasma membranes for the transport of materials into and out of a cell?

The proteins allow a cell to select what compound will be transported, meeting the needs of the cell and not bringing in anything else.

Why do ions have a difficult time getting through plasma membranes despite their small size?

Ions are charged, and consequently, they are hydrophilic and cannot associate with the lipid portion of the membrane. Ions must be transported by carrier proteins or ion channels.

Glossary


Why is phagocytosis not included as a type of receptor-mediated endocytosis? - Biology

Receptor-Mediated Endocytosis

Blake R. Peterson, Department of Chemistry, The Pennsylvania State University, University Park, Pennsylvania

Specific receptors on the surface of mammalian cells actively internalize cell-impermeable ligands by the mechanism of receptor-mediated endocytosis (RME). This process is critical for the acquisition of nutrients, signal transduction, development, neurotransmission, and cellular homeostasis. Binding of ligands to internalizing receptors on the plasma membrane results in clustering of the complex in clathrin-coated pits or other dynamic membrane regions. Invagination of these regions yields intracellular vesicles that fuse to form membrane-sealed endosomes. Receptors typically dissociate from ligands in these acidic compartments, which allows the free receptor to cycle back to the cell surface, whereas ligands are often degraded on delivery to lysosomes, which liberates amino acids and other nutrients. By mimicking endogenous ligands, certain protein toxins, viruses, and other pathogens exploit RME to enter the cytoplasm or reach other intracellular destinations. Similarly, artificial delivery systems that mimic ligands or receptors can enhance efficiently the cellular uptake of impermeable molecules, including drugs, proteins, and nucleic acids. Advances in small-molecule probes, structural biology, and genetic methods are beginning to illuminate the complex mechanisms of this process at the molecular level.

The plasma membrane of eukaryotic cells encapsulates the inner cellular machinery, thereby protecting fragile biologic structures from potentially toxic or opportunistic extracellular materials. Only small hydrophobic molecules can penetrate rapidly this lipid bilayer through passive diffusion. More polar essential amino acids, sugars, and ions access the cell interior by interacting with membrane proteins that function as selective pumps or channels. For many other cell-impermeable small molecules, macromolecules, and particles to access the cell interior, cells must facilitate uptake actively, with regions of the plasma membrane functioning to capture solutes by invaginating and pinching off to form intracellular vesicles. This process is termed endocytosis, which represents multiple related mechanisms for the internalization of extracellular molecules (1). Endocytosis is divided into two primary categories: phagocytosis (cell eating) and pinocytosis (cell drinking). Phagocytosis enables the uptake of large particles, including intact bacteria and yeast, through an actin-mediated mechanism that is generally restricted to specific cell types, such as macrophages, monocytes, and neutrophils. Pinocytosis, by contrast, occurs in all nucleated mammalian cells and involves the active invagination of small regions of cellular plasma membranes to capture solutes within vesicles of less than 200 nm in diameter. These vesicles fuse in the cytoplasm to form membrane-sealed compartments termed endosomes, and their contents are sorted to allow trafficking to specific destinations. Pinocytosis can involve the nonspecific uptake of extracellular fluid, as well as the uptake of specific molecules in the extracellular environment, mediated by receptors on the plasma membrane. Some mechanisms of endocytosis operate rapidly and continuously. In cultured fibroblasts, under physiologic conditions, membrane equivalent to the entire cell surface is perpetually internalized with a half-life of 15 to 30 minutes (2). Most pinocytic pathways involve specific interactions of receptors with ligands. In receptor-mediated endocytosis (RME), internalizing receptors on the cell surface bind cell-impermeable ligands to concentrate ligands in the cell. This mechanism is thousands of times more efficient than nonspecific pinocytosis for the cellular acquisition of nutrients and other impermeable molecules. The receptors involved in RME comprise a structurally diverse group of biomolecules that project ligand-binding motifs into the extracellular environment. Cell-impermeable small molecules, lipids, peptides, proteins, nucleic acids, and carbohydrates are internalized by RME, which enables the consumption of nutrients, elimination of pathogens, and termination of signals initiated by extracellular stimuli. RME followed by subsequent exocytosis of the ligand from one side of the cell to another is termed transcytosis, and this mechanism allows the delivery of nutrients across membrane barriers, such as the blood-brain barrier (3). By exploiting RME, certain viruses, protein toxins, and other pathogens invade cells and cause disease (4). However, to our benefit, drug and other delivery systems that mimic properties of ligands or receptors can be used to access these natural pathways across biologic membranes (5-8).

Internalizing Cell-Surface Receptors and Their Ligands

Cell-surface receptors involved in RME range from macromolecular proteins, which span the plasma membrane, to small glycolipids, which are anchored only to the plasma membrane outer leaflet. Structural representations of several receptors and ligands involved in this process are shown in Fig. 1. X-ray crystal structures of the extracellular domains of the low density lipoprotein (LDL) receptor (9), the transferrin receptor (TFR) (10), the human growth hormone receptor (11), the bovine rhodopsin (12), and the FcyRIIIB (CD16) (13) are shown as part of a composite image that illustrates the nature of attachment of the receptor to the plasma membrane. The small glycolipid receptor ganglioside GM1 is shown to the right, rendered as a molecular model (14). Structures of cognate ligands are positioned above or as a complex with receptor extracellular fragments. These ligands include the structure of LDL determined by cryoelectron microscopy (shown reduced in scale compared with the receptor) (15), transferrin, human growth hormone, the Fc fragment of human IgG, and cholera toxin (16). Brief descriptions of these and related receptors and ligands are provided in the following sections. Other representative examples of receptors and ligands involved in RME are listed in Table 1.

The LDL receptor: a macromolecular membrane-spanning protein critical for cellular uptake of cholesterol

Uptake of cholesterol-laden LDL particles by the LDL receptor (LDLR, Fig. 1) is one of the best-characterized examples of RME (9, 17-18-19). The mature LDL receptor is a single pass transmembrane glycoprotein of 839 amino acids (

115KDa, Fig. 1). LDL ligands are characterized as particles of

2500 KDa) that comprise a core of

1500 molecules of cholesterol esters, esterified primarily by linoleic acid, encapsulated by a monolayer of free cholesterol, phospholipids, triglycerides, and a single large protein termed apolipoprotein B-100 (apo-B,

550KDa). By recognizing the protein component of LDL, the LDLR enables cells in all tissues of vertebrate animals to internalize exogenous cholesterol, which is a key building block required for the biosynthesis of steroid hormones, bile acids, and cellular membranes. By interacting with the protein clathrin, which forms coated pits on the cytosolic face of the plasma membrane, the LDLR constitutively delivers LDL into endosomes, followed by cycling of the receptor back to the cell surface. Inherited mutations in the LDLR that disrupt endocytosis, and thereby increase serum LDL, have been shown to accelerate atherosclerosis in patients with familial hypercholesterolemia (17). Rapidly proliferating cells have a particularly high demand for cholesterol because mammalian plasma membranes are composed of one-third protein and two-thirds lipid plus

30% of the cellular plasma membrane lipids are cholesterol (20). For this reason, the LDL receptor is often overexpressed on cancer cells, and LDL receptors provide a target for the selective delivery of anticancer and tumor imaging agents (21, 22). The LDLR is also a portal exploited by Hepatitis C virus and other Flaviviridae viruses to penetrate into cells (23).

The transferrin receptor: a homodimeric transmembrane protein that enables cellular uptake of iron

Iron is an essential nutrient that functions as an enzyme cofactor in redox reactions and plays a structural role through ligand coordination. Under physiologic conditions, iron can be converted readily between the ferrous (Fe 2+ ) and the ferric (Fe 3+ ) oxidation states. However, ferrous iron is dangerous to living cells because it can generate hydroxyl radicals that oxidatively damage proteins, nucleic acids, and lipids. Additionally, iron in the ferric (Fe 3+ ) oxidation state forms a highly insoluble hydroxide complex that is not readily available to cells. In vertebrate animals, ferric iron is transported in serum bound to the protein transferrin (TF), which is a bilobed glycoprotein of 80 KDa in humans (Fig. 1) (10). This protein binds Fe 3+ using a synergistic anion, typically carbonate, two Tyr, one His, and one Asp residue. Cellular uptake of TF is mediated by the transferrin receptor (TFR, Fig. 1), which is a homodimeric transmembrane protein of 85 KDa in humans that binds two diferric transferrin ligands. Internalization of TF by RME results in the release of Fe 3+ in acidic endosomal compartments. However, the apo-TF remains bound to TFR, the receptor-ligand complex cycles back to the plasma membrane, and apo-TF is released from the TFR at neutral pH. Ferric iron is reduced to the ferrous state within endosomes, and the iron transporter DMT1 delivers the Fe 2+ ion into the cytoplasm. Like the LDLR, the TFR is upregulated on certain cancer cell lines, and drugs conjugated to transferrin have been used as targeted delivery systems (5). In mice, the mouse mammary tumor virus exploits the TFR to enter cells (24).

Figure 1. Representative structures of receptors and ligands involved in receptor-mediated endocytosis. The gray bar at the bottom of the figure represents the cellular plasma membrane. From left to right, X-ray crystal structures of the extracellular domains of the human LDL receptor, the human transferrin receptor, the human growth hormone receptor, bovine rhodopsin, and FcyRNIB are shown illustrating the nature of attachment to the plasma membrane. A molecular model of the glycolipid ganglioside GM1 is on the far right. A structure of LDL determined by electron cryomicroscopy (27 A resolution) is shown on the upper left (not drawn to scale image courtesy of Dr. Wah Chiu, Baylor College of Medicine). Other ligands shown from left to right include receptor-bound transferrin, receptor-bound human growth hormone, receptor-bound Fc region of human IgG, and the B-subunit of cholera toxin.

Receptors for Growth Factors and Hormones

Human growth hormone (GH1, Fig. 1), epidermal growth factor (EGF), insulin (INS), platelet-derived growth factor (PDGF), and many cytokines bind receptors that activate intracellular tyrosine kinase activity. The major isoform of GH1 is a protein of 191 amino acids (22 KDa) that functions in part to stimulate the growth of bone and internal organs in children. As shown in Fig. 1, the human growth hormone receptor (GHR), which is a member of the cytokine-hematopoietin receptor superfamily, comprises a transmembrane glycoprotein of 620 amino acids (130 KDa) (25). Binding of GH1 results in dimerization and conformational changes in the GHR that initiate cellular signaling via recruitment and activation of tyrosine kinases. The GHR is internalized constitutively via clathrin-coated pits, and both this receptor and its ligand are degraded by proteolysis in lysosomes, which provides a mechanism to terminate the extracellular signal. The receptors for EGF and insulin are receptor tyrosine kinases (RTKs) that become internalized only upon binding of ligands. The EGFR family of RTKs includes EGFR (HER1, erbB-1), HER2 (erbB-2), HER3 (erbB-3), and HER4 (erbB-4). Upregulation of expression or the production of activating mutants of this family is known to cause several cancers (26). By binding its extracellular domain, the FDA-approved monoclonal antibody drug Herceptin downmodulates HER2, thereby inhibiting the proliferation of the subset of breast cancers that overexpress this receptor.

G-protein-coupled receptors

G-protein-coupled receptors (GPCRs), also known as seven transmembrane receptors (7TMs), are the largest known superfamily of proteins. They are involved in all types of responses to stimuli, from intercellular communication to the senses of vision, taste, and smell. They respond to diverse ligands ranging from photons (e.g., rhodopsin, Fig. 1) to small molecules (e.g., binding of epinephrine to the β2-adrenergic receptor) and proteins (e.g., chemokine receptors). Binding of ligands to the extracellular or transmembrane domains of these proteins causes conformational changes that relay a signal to intracellular G proteins that trigger additional cellular responses. Many GPCRs undergo RME by binding to intracellular arrestin proteins that associate with clathrin. The importance of GPCRs in normal biologic processes and disease has made this family of proteins the target of up to 50% of all modern drugs.

Receptors anchored to the plasma membrane by lipids: Glycosylphosphatidylinositol (GPI)-anchored proteins and glycolipids

Some cell-surface receptors are attached to the plasma membrane by lipids that penetrate only into the outer leaflet of the bilayer. Posttranslational modification of proteins with GPI-lipids allows proteins such as folate receptor-2 (FOLR2) to attach to the cell surface and promote RME of the vitamin 5-methyltetrahydrofolate. Folate receptors are upregulated in certain cancers, and folate derivatives have been linked to drugs and molecular probes to treat and image certain tumors. The related GPI-linked receptor FcyRIIIB (CD16, 26.2KDa, Fig. 1) is involved in the immune response. This receptor binds the invariant Fc region of immunoglobulin-G to promote RME of this ligand. Much smaller glycolipids also participate in RME. Gan- glioside GM1 (Fig. 1), a 1.6 KDa glycolipid, enables the protein cholera toxin (16) and the nonenveloped virus SV40 to penetrate into cells upon binding to its pentasaccharide headgroup (27).

Because of the lack of a direct connection to clathrin via a cytoplasmic region, the endocytosis of GPI-linked proteins and other lipid-linked receptors is slower than the uptake of most transmembrane proteins. Instead of clathrin-mediated endocytosis, the internalization of many lipid-linked receptors has been proposed to involve distinct membrane subdomains termed lipid rafts (28). These domains are enriched in cholesterol and sphingolipids and in some cell types include flask-shaped invaginations termed caveolae (29, 30). Many proteins covalently or noncovalently associated with cholesterol, sphingolipids, or saturated lipids are thought to associate with lipid rafts that segregate and concentrate membrane proteins, regulate signal transduction pathways (31), and control the endocytosis of specific receptors (32). Protein toxins and viruses often exploit receptor-mediated endocytosis involving lipid rafts or clathrin to penetrate into the cell interior (4).


Exocytosis

Exocytosis is the opposite of the processes we discussed above in that its purpose is to expel material from the cell into the extracellular fluid. Waste material is enveloped in a membrane and fuses with the plasma membraneʼs interior. This fusion opens the membranous envelope on the cellʼs exterior, and the waste material expels into the extracellular space. Other examples of cells releasing molecules via exocytosis include extracellular matrix protein secretion and neurotransmitter secretion into the synaptic cleft by synaptic vesicles(Figure 17.6).

Figure 17.6: Exocytosis - vesicles containing substances fuse with the plasma membrane. The contents then release to the cell&rsquos exterior. (Kindred Gray 2020 via LibreTexts CC BY 4.0 Adapted from Biology 2e)


What is phagocytosis?

Image 1: Phagocytosis: The detection of target material

The detection of target material begins when a cell senses target material on its surface (Image 1). Most cell types have a dedicated set of cell surface receptors that recognize various substances. For example, immune cells can sense invasive microbes with receptors that recognize pathogen-associated markers. After the target material has been detected, the cell surface receptor initiates a series of signals that prepare the cell for phagocytosis.

Image 4: Phagosome maturation. Here, the phagosome has merged with a lysosome, forming a phagolysosome.


Maturation of the phagosome is the final phase of phagocytosis (Image 4). Phagosome maturation consists of a series of material handoffs between the original phagosome and cellular compartments specialized in digestion. The early stages of phagosome maturation include a combination of fusion and fission events that prepare the cellular membrane of the maturing phagosome for material digestion. During the final stages of phagocytosis, the internal environment of the mature phagosome becomes more acidic and reactive, which aids the digestion of target material such as microorganisms.

What is pinocytosis?

While phagocytosis involves the ingestion of solid material, pinocytosis is the ingestion of surrounding fluid(s). This type of endocytosis allows a cell to engulf dissolved substances that bind to the cell membrane prior to internalization. Unlike phagocytosis, pinocytosis is a “drinking” mechanism wherein a cell actively engulfs external fluids over time. Even though pinocytosis differs from other forms of receptor-mediated endocytosis, these terms overlap with one another due to their similarities.

Pinocytosis function


In humans, pinocytosis primarily occurs when cells absorb nutritional or waste droplets suspended in external fluid. The nutritional molecules that can activate pinocytosis include fats, sugars, proteins, ions or other small molecules. This process begins when a soluble substrate binds to the surface of a cell (image B1)

The size of these vesicles during the intake of fluid material can establish whether a cell performs macropinocytosis vs micropinocytosis. Macropinocytosis is a form of non-specific endocytosis that is common for all cell types. This process includes the intake of fundamental nutrients such as amino acids, carbohydrates and fats.

Micropinocytosis involves the ingestion of fluid material by small vesicles that are typically no larger than 0.1 micron. This process is typically initiated by cell surface lipid domain once they bind to their specific target molecules.

Phagocytosis vs pinocytosis: chart


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, the cell's uptake of substances targets a single type of substance that binds to the receptor on the cell membrane's external surface. (credit: modification of work by Mariana Ruiz Villareal)

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.

Link to Learning

See receptor-mediated endocytosis in action, and click on different parts for a focused animation.


Difference Between Endocytosis and Phagocytosis

Cells are said to be the functional unit of organisms such as in humans and animals. Cells are very important among organisms since these constitute the tissues, which constitute the muscles, then organs, followed by body systems.

A cell has its different parts with different functions. Students are already aware of this as early as elementary school. Common parts and functions include: the mitochondria which is the powerhouse of the cell, the lysosomes which are like food storage and much more.

Absorption of nutrients such as proteins, carbohydrates, fats, and other molecules occur at the cellular level. This process happens through endocytosis, exocytosis, and a more specific way is through phagocytosis. Let us try to differentiate “endocytosis” from “phagocytosis.”

“Endocytosis” is defined as the process of engulfing molecules. It has four subcategories which are the clathrin-mediated endocytosis, caveolae, macropinocytosis, and phagocytosis. Phagocytosis, on the other hand, is the process of engulfing nutrients with a particular size only which is 0.75 nanometers in diameter. Examples of these are: dust particles, cell debris, and apoptotic cells.

Clathrin-mediated endocytosis involves molecules that are 100 nanometers in diameter in order for them to absorb and digest. Caveolae, on the other hand, absorbs particles that are less than 50 nanometers. Lastly, macropinocytosis engulfs particles sized 0.5-5 nanometers.

Phagocytosis came from the Greek word “phagein” meaning “to devour,” “kytos” meaning “cell” and “-osis” meaning “process” which is totally defined as the process of engulfing solid particles. “Endocytosis” came from the word “endo,” which means “within,” “cyt” meaning “cell” and “-osis” meaning “process.”

Phagocytosis involves the engulfing of solid particles which only can be done through oxygen or non-oxygen dependent processes while endocytosis involves either solid or liquid particles.

1.“Phagocytosis” is under “endocytosis.” Endocytosis has four subcategories which include: phagocytosis, clathrin-mediated endocytosis, macropinocytosis, and caveolae.
2.“Phagocytosis” came from the Greek word “phagein” meaning “to devour,” “kytos” meaning “cell” and “-osis” meaning “process” which is totally defined as “the process of engulfing solid particles.” “Endocytosis” came from the word “endo” which means “within,” “cyt” meaning “cell,” and “-osis” meaning “process.”
3.Phagocytosis involves the engulfing of solid particles which only can be done through oxygen or non-oxygen dependent processes while endocytosis involves either solid or liquid particles.


Watch the video: Pinocytosis, Phagocytosis and Receptor-Mediated Endocytosis (November 2021).