Which step in endocytosis requires ATP?

Which step in endocytosis requires ATP?

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Everybody seems to agree that endocytosis is an energy-using process, and as such requires ATP hydrolysis. However, which particular step requires it? More precisely, which 'molecular machine' involved in endocytosis requires ATP? I cannot seem to find a good answer in the literature.

Endocytosis (specifically you asked about clathrin-mediated endocytosis) is indeed an energy consuming process. the coating of the vesicle may be "spontaneous", but the pinching off of the vesicle, the uncoating of the clathrin, and the transportaion of the vasicle inside the cell all require ATP/GTP hydrolysis.

Dynamin - dynamin forms a spiral around the neck of the vesicle, and uses GTP hydrolysis which in order tighten the coil around the vesicle neck causes it to break and results in the pinching off of the vesicle from the parent membrane.

The uncoating of the clathrin is also ATP/GTP consuming. proteins such as hsp70 chaperon and auxilin is thought to be involved in the ATP hydrolysis. the uncoating process starts after the pinching off of the vesicle.

the tranportation of the vesicle will also cost energy, proteins such as the Myosin family are considered to transport endocytic vesicles into the cell, and use ATP hydrolysis.

Dynamin - Wiki

Myosin - Wiki

Uncoating process - Molecular Biology Of The Cell ed.6 p.701


Endocytosis is the process of bringing substances inside a cell from the external environment with the help of the cell membrane. Through this method, cells acquire nutrients required for growth and reproduction. It is a form of the active transport mechanism and thus needs energy, in the form of ATP, to proceed.

The word ‘endocytosis’ is derived from the Greek words ‘endon’, meaning ‘within’, ‘kytos’, meaning ‘cell’, and ‘-osis’, meaning ‘process’. The process was first proposed and described by cytologist Christian De Duve in 1963.

Examples of Substances Transported Using the Process

Substances like fluids, electrolytes, proteins, and other macromolecules are taken up inside the cell using endocytosis.

Active Vs Passive Transport

The movement of substances in and out of the cell without any energy input is known as passive transport. Generally, this involves the movement of molecules/ions from a region of high concentration (e.g. high concentration of molecules or ions in the extracellular environment) to an area of low molecule/ion concentration (e.g. inside the cell). The molecules or ions simply diffuse through the membrane to enter or leave the cell.

Active transport, on the other hand, requires the utilization of energy in the form of ATP for molecules/ions to be transported in or out of the cell. As mentioned, endocytosis is a type of active transport given that energy is required for molecules/substances to be transported into the cell.

ATP molecules have to bind to proteins on the cell which causes them to undergo a conformational change. This is an important activity that helps to cause the change in the shape of the membrane that contributes to the formation of vesicles. This allows for the molecules/substances of interest to be engulfed and transported into the cell.

There are three main types of endocytosis which include:


SMase-induced, ATP-independent Vesicle Formation in J774 Macrophages

Fig. 1,a shows the uptake of a fluid endocytosis marker, FITC-dextran, by J774 cells during a 10-min incubation at 37°C. These control cells internalize FITC-dextran and deliver it to endosomes that are seen as bright fluorescent dots. As expected, this uptake is blocked when cellular ATP is depleted by preincubation with sodium azide and 2-deoxyglucose (Fig. 1,b). Under the conditions used for Fig. 1,b, cellular ATP is 2.4 ± 0.5% of control values, as determined by an ATP luminescence assay. When ATP-depleted cells are treated with SMase (50 mU/ml), there is substantial uptake of FITC-dextran into the cells (Fig. 1,c). SMase treatment had no effect on cellular ATP levels. To determine whether FITC-dextran is in sealed vesicles, these cells were either chased in dextran-free medium for long periods of time, or exposed to trypan blue, a membrane-impermeant quencher of FITC fluorescence (Hed et al., 1987). FITC-dextran labeling was not reduced after a 60-min chase, and the fluorescence was not quenched by 2 mg/ml trypan blue (data not shown). It has been shown previously that trypan blue is able to quench fluorescence even in deep surface invaginations (Myers et al., 1993), and the lack of quenching is strong evidence for the sealing of the SMase-induced vesicles. As seen in Fig. 1 c, these vesicles remain in the cell periphery, consistent with the requirement for ATP-dependent motor proteins such as dynein for translocation of vesicles along microtubules into the center of a cell (Holzbaur and Vallee, 1994). When ATP is restored to the cells, these vesicles move rapidly into the center (see below).

To visualize the SMase-induced vesicles by electron microscopy, ATP-depleted J774 cells were incubated for 10 min with HRP and 50 mU/ml SMase. Internalized HRP is visualized after diaminobenzidine treatment as a dark precipitate. As shown in Fig. 2, SMase treatment induces the formation of numerous vesicles that are typically 50–500 nm in diameter and marked by diaminobenzidine reaction product precipitate along the lumenal face of the vesicle membranes. There was not a significant difference in either the size distribution or number of vesicles when the incubation time was reduced from 10 to 2.5 min (data not shown). This suggests that the formation of vesicles is complete in a few min after exposure to SMase. The SMase- induced vesicles exhibit only peripheral staining, and no internal vesicles are seen. We did not observe a discernible coat on the vesicles.

SMase-induced Vesicle Formation in Fibroblasts

The formation of vesicles in response to SMase is also observed in the TRVb-1 line derived from CHO fibroblasts. An advantage to using CHO cells is that they are less active in fluid uptake compared with macrophages, so the effect of SMase can be examined even in the absence of energy poisons. During a short incubation with FITC-dextran (2.5 min) little uptake is observed in control cells (Fig. 3,a). When SMase is added to these energy-replete cells, there is a burst of vesicle formation (Fig. 3,b), similar to the vesicles induced by SMase treatment of ATP-depleted cells (Fig. 3, c and d). Therefore, SMase-induced vesicle formation does not require ATP depletion, although we have shown that SMase-induced vesicle formation is an ATP-independent event. SMase-induced vesicles in energy-replete TRVb-1 cells (Fig. 3 b) were observed in the cell periphery because of the short incubation (2.5 min) vesicle formation because of SMase is completed within 5 min (earliest time point examined). Electron microscopy using HRP showed that the SMase-induced vesicles in TRVb-1 cells were structurally similar to those in J774 cells (data not shown).

To further verify that SMase-induced vesicle formation is indeed ATP independent, TRVb-1 cells were incubated with sodium azide/2-deoxyglucose and then permeabilized with SL-O before being exposed to SMase. Cellular ATP level in these cells after SMase treatment was down to 0.07 ± 0.01% of the level in intact, untreated cells. In response to SMase treatment, the SL-O–permeabilized cells took up a fluid-phase marker, Lucifer yellow in this experiment, into peripheral vesicles (Fig. 4,a). SL-O permeabilization of ATP-depleted cells without SMase did not induce vesicle formation (data not shown). SMase-treated cells were able to retain Lucifer yellow (mol wt 457) after a 2-h chase in a dye-free medium (Fig. 4 b), indicating these vesicles are completely sealed off from the plasma membrane.

To verify that the observed effects of SMase were because of SMase enzyme activity, we tested another SMase from a different bacterial source. SMase from Staphylococcus aureus had the same effect on TRVb-1 cells and J774 cells as the SMase from Bacillus cereus. Furthermore, when the SMase preparation was size-fractionated by fast protein liquid chromatography, the vesicle-forming activity copurified with the SMase activity (data not shown).

Kinetics of SMase-induced Vesicle Formation

To determine the kinetics of SMase-induced vesicle formation, J774 macrophages were incubated with FITC-dextran with or without SMase for different lengths of time, and total dextran uptake per cell was measured by quantitative fluorescence microscopy. Results are shown in Fig. 5. As expected, in energy-replete cells treated with or without SMase (inset), the uptake of dextran increased approximately linearly with time. ATP depletion completely blocked dextran internalization in control cells (closed squares), but SMase treatment of ATP-depleted cells caused a rapid burst of dextran uptake (closed circles) that is complete within 10 min (earliest time point examined). Cells apparently became insensitive to SMase after the initial burst since longer exposure (>10 min) to SMase did not result in additional internalization. FITC-dextran uptake kinetics in TRVb-1 cells were similar to those of J774 cells (data not shown). The amount of FITC-dextran uptake induced by SMase in TRVb-1 cells during a 5-min incubation was equivalent to the fluid uptake by energy- replete cells over a 20–30-min incubation.

Characterization of the Membrane Structures in SMase-induced Vesicles

To determine the extent of plasma membrane internalization caused by SMase treatment, a fluorescent membrane-lipid analogue, C6-NBD-gal, was used to label the plasma membrane of TRVb-1 cells. Cells were incubated on ice with C6-NBD-gal, depleted of ATP, and then treated with or without SMase. As shown in Fig. 6, in the absence of SMase the plasma membrane was relatively uniformly labeled by C6-NBD-gal (a), and a backexchange in BSA-containing medium extracted most of this surface label (b). SMase-treated cells (c) show more punctate labeling than untreated cells. After surface C6-NBD-gal was removed by backexchanging in BSA-containing medium, the peripheral punctate labeling of the SMase-treated cells is retained (d). This retained C6-NBD-gal label resembles the FITC-dextran uptake pattern in SMase-treated cells (Fig. 3 d). The fact that C6-NBD-gal in SMase-induced vesicles is not available for backexchange provides further evidence that these vesicles are completely sealed off from the extracellular environment. After quantifying C6-NBD-gal fluorescence images, we find that 30 ± 5% (average of five fields of cells ± SD) of the plasma membrane C6-NBD-gal is internalized in response to SMase. In parallel experiments using a spectrofluorometer to detect C6-NBD-gal extracted from solubilized cells, we find that 14 ± 7% of the C6-NBD-gal label is resistant to backexchange after treatment with SMase. The difference between the results obtained by fluorometry and digital microscopy may be explained by a small population of cells that take up a large amount of C6-NBD-gal throughout the cell even on ice (c). C6-NBD-gal in these cells can be extracted by backexchange. The fluorescence intensity of these cells, therefore, contributes to the total fluorescence intensity in the spectrophotometric analysis but not the microscopic analysis, and this may account for the difference in the values obtained from these two methods. Nevertheless, the results obtained by both methods show that the amount of membrane internalized is much greater than the area covered by clathrin-coated pits and/or caveolae, which typically comprise only 2–4% of the plasma membrane. The total intensities of the membrane C6-NBD-gal labeling of ATP-depleted cells with or without SMase treatment are not significantly different, indicating that SMase induces endo- but not exovesiculation.

SMase-induced vesicles are formed from part of the plasma membrane, raising the question as to whether they are from some specialized or invaginated plasma membrane regions. To address this, we examined if clathrin or caveolae were preferentially associated with these vesicles. TRVb-1 fibroblasts were treated with SMase in the presence of FITC-dextran, fixed, permeabilized, and stained with antibodies against clathrin or adaptor protein 2 (AP2). We did not find any significant enrichment of either clathrin or AP2 in FITC-dextran–containing vesicles by immunofluorescence microscopy (data not shown). When SMase-treated cells were colabeled with antibody to caveolin/ VIP-21, the major protein in caveolae, there was no significant colocalization between caveolin and FITC-dextran (data not shown). SMase-induced vesicles, therefore, appear to not be enriched in either clathrin-coated pits or caveolae.

Sorting of Membrane and Fluid Content in SMase-induced Vesicles

We next investigated the fate of internalized receptors and the fluid contents of SMase-induced vesicles. J774 cells were preincubated with TRITC-dextran to label the late endosomes and lysosomes. The cells were then energy-poisoned and incubated with SMase and FITC-dextran. After 10 min, cells were rinsed and chased for an additional 60 min either in complete medium that allows restoration of ATP, or in the continued presence of energy poisons. In the continuous presence of energy poisons, SMase-induced vesicles (FITC-dextran–containing vesicles) remained in the cell periphery (Fig. 7,a), well separated from the TRITC-dextran–labeled late endosomes and lysosomes (Fig. 7,b). When ATP was restored, however, the FITC dextran in the SMase-induced vesicles moved into the cell and merged with TRITC-dextran–containing compartments (Fig. 7, c and d), indicating that these vesicles are able to deliver FITC-dextran to the previously formed late endosomes and lysosomes.

To test if the SMase-induced vesicles are also able to sort receptors for recycling, Cy3-transferrin was bound onto the surface of ATP-depleted J774 cells. The cells were then treated with SMase in the presence of FITC-dextran. Transferrin that remained on the cell surface was stripped off with a mild acid wash (Salzman and Maxfield, 1988). As shown in Fig. 8, Tf and dextran were initially internalized into the same compartments after SMase treatment (Fig. 8, a and b). When the cells were returned to complete medium in the absence of energy poisons, the Tf (Fig. 8,d) was rapidly sorted away from the FITC-dextran compartments (Fig. 8 c) and returned to the cell surface. Thus, the contents of the SMase-induced vesicles can be sorted with recycling receptors returned to the cell surface and the remaining contents being delivered to late endosomes.

Ceramide Is Included in SMase-induced Vesicles

To understand the mechanism of SMase-induced vesicle formation, it would be useful to know the lipid composition of these vesicles. As a start on these studies, we have used a fluorescent sphingomyelin to determine if ceramide formed from it enters the induced vesicles. We incorporated BODIPY-C12-SM into the plasma membrane of TRVb-1 cells. When cells were exposed to SMase, a significant fraction of the BODIPY fluorescence translocated to the Golgi region (Fig. 9,a). This is consistent with the behavior of fluorescent acyl chain derivatives of ceramide that have been shown to be transported to the Golgi apparatus by a nonvesicular mechanism (Martin and Pagano, 1994). The sphingomyelin analogue itself does not translocate to the Golgi as demonstrated by the cells in Fig. 9,b, which were incubated at 37°C for the same time as the cells in Fig. 9,a, but without SMase exposure. It is evident that under our experimental conditions, SMase hydrolyzed the majority of BODIPY-C12-SM and turned it into BODIPY-C12-ceramide that could translocate to the Golgi. Since the transport of fluorescent ceramides is thought to occur via flipping to the cytoplasmic leaflet and binding to cytoplasmic carrier proteins, it should be blocked by removal of such proteins. This would allow us to observe the presence of the ceramide in SMase-induced vesicles. We permeabilized BODIPY-C12-SM–labeled cells with SL-O to remove cytosol proteins. As shown in Fig. 9,d, SMase treatment in these cells caused BODIPY fluorescence to leave the plasma membrane and, significantly, to concentrate in SMase-induced vesicles that were labeled by rhodamine-dextran (Fig 9 c). Taken together, these studies indicate that a substantial amount of the BODIPY ceramide formed by SMase enters the induced vesicles, and this BODIPY-C12-ceramide can flip to the cytoplasmic leaflet.


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 vacuole that is formed from the plasma membrane.

Figure 3.30 Three variations of endocytosis are shown. (a) In one form of endocytosis, phagocytosis, the cell membrane surrounds the particle and pinches off to form an intracellular vacuole. (b) In another type of endocytosis, pinocytosis, the cell membrane surrounds a small volume of fluid and pinches off, forming a vesicle. (c) In receptor-mediated endocytosis, uptake of substances by the cell is targeted to a single type of substance that binds at the receptor on the external cell membrane.

Phagocytosis is the process by which large particles, such as cells, are taken in by a cell. For example, when microorganisms invade the human body, a type of white blood cell called a neutrophil removes the invader through this process, surrounding and engulfing the microorganism, which is then destroyed by the neutrophil (Figure 3.30).

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 process takes in solutes that the cell needs from the extracellular fluid (Figure 3.30).

A targeted variation of endocytosis employs binding proteins in the plasma membrane that are specific for certain substances (Figure 3.30). The particles bind to the proteins and the plasma membrane invaginates, bringing the substance and the proteins into the cell. If passage across the membrane of the target of receptor-mediated endocytosis is ineffective, it 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 a 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 the chemical from their blood.

What is clathrin-mediated endocytosis?

Clathrin-mediated endocytosis (CME) is a vesicular transport event that facilitates the internalization and recycling of receptors engaged in a variety of processes, including signal transduction (G-protein and tyrosine kinase receptors), nutrient uptake and synaptic vesicle reformation [1] . Two classical examples of CME are iron-bound transferrin recycling and the uptake of low-density lipoprotein (LDL).

A. Clathrin is a triskelion shaped scaffold protein. B. Clathrin assembles to form a coat around a mature vesicle. C. Formation of the clathrin coated vesicle requires changes in membrane curvature, which is driven by PIP2 levels and BAR protein binding.

CME is characterized by the involvement of clathrin, which is a triskelion-shaped scaffold protein composed of three heavy and three light chains [2] [3] [4] . Clathrins polymerize around the cytoplasmic face of the invaginated membrane and act as a reinforced mould in which the membrane vesicle may form without direct association with the membrane [5] . Dissociation of the coat occurs rapidly following scission of the vesicle from the membrane.

Initiation of the clathrin complex formation requires the accumulation of phosphatidylinositol𔂮,5‑bisphosphate (PIP2) and adaptor proteins, such as AP-2, at the pinching site [6] [7] [8] . In the case of clathrin-coated vesicles (CCV) formed at the trans-Golgi apparatus (TGA), AP-1 is essential [9] [10] .

Growth of the clathrin coated pit requires BAR (Bin/Amphiphysin/Rvs) domain proteins [11] [12] [13] and reorganization of the actin network [14] . The final scission step involves BAR domain proteins, dynamin and the dephosphorylation of PIP2. The latter step is suggested to function within a positive feedback loop, with regards to phosphatase activity [15] [16] [17] . The vesicles are then transported and sorted, based on receptor type or membrane composition [18] , to the various destinations including the trans-Golgi network, endosomes and vacuoles.

ACTIVE TRANSPORT - Sodium and Potassium Pump, Endocytosis and Exocytosis.

In many cases, cells must move materials up their concentrated gradient, from and area of lower concentration to an area of higher concentration. Such movement of materials is known as ACTIVE TRANSPORT. Unlike passive transport, active transport requires a cell to use energy (ATP).
Active transport is very similar to that of facilitated diffusion for it uses transport proteins to allow molecules to pass through the cell membrane. However, the difference this time is that the ion or molecules physical binds to the protein and then is pumped across the membrane.

Cells often move molecules across the membrane AGAINST a Concentration Gradient. These molecules or ions go form an area of LOW concentration to areas of HIGH concentration.
To move molecules AGAINST the concentration gradient REQUIRES ENERGY. (Active transport)
The CARRIER PROTEINS act as PUMPS that USE ENERGY to move IONS and MOLECULES across the membrane. The carrier proteins that serve in active transport are often called CELL MEMBRANE PUMPS. Active transport is especially important in maintaining ion concentration in the cell and between cells.

SODIUM-POTASSIUM PUMPS are important for muscle contractions, the transmission of nerve impulses, and the absorption of nutrients. Sodium-Potassium pumps in animal cells pump sodium ions out and potassium ions in, against (up) the concentration gradient. ATP supplies the energy needed by the carrier proteins to do this job. (See diagram in textbook.)

In Plants, ACTIVE TRANSPORT enables roots to absorb nutrients from the soil. Plant nutrients are more concentrated inside the roots than in the surrounding soil. Without active transport, nutrients would diffuse out of the roots. Active Transport in the root cell membrane enables the plant to absorb the nutrients against the
Concentration Gradient.

Some molecules, such as COMPLEX PROTEINS, are too LARGE to cross the cell
membrane. In order for these molecules to cross the membrane they need something to transport them. These proteins are too large even to fit through the protein channels, so the cell must use a unique technique called BULK TRANSPORT.
In BULK TRANSPORT, large molecules, food, and other substance are packed in membrane-bound sacs called a vesicle, and these move across the cell membrane.
There are several types of bulk transport, including ENDOCYTOSIS,

During ENDOCYTOSIS the Cell Membrane folds into a POUCH that encloses the particles. (Figure 1.40 in text). The Pouch pinches off INSIDE the Cell to form a VESICLE/ VACULE (membrane-wrapped bubbles).
The VESICLE/ VACULE can then fuse with other organelles (lysosomes) or release its contents into the cytoplasm.


PINOCYTOSIS is sometimes called “CELL DRINKING". This involves the intake of a small droplet of ECF, together with any dissolved substances or small particles that it may contain. This happens in nearly all cells, and occurs all the time.

The Food Vesicle can then Fuse with a LYSOSOME that contains DIGESTIVE ENZYMES.
White Blood Cells (WBC, PHAGOCYTES) Destroy Bacteria and other Unwanted Cells by

Products MADE IN the Cell are Packaged in GOLGI VESICLES, which then FUSE with the Cell Membrane and Secrete Material OUT OF THE CELL.


mr smith can you pleeeeease post the review questions

hi mr.smith,
i have 2 questions, do we have to know how to draw a sodium-potassium pump diagram? and why is the fluid-mosaic modle important to cells?

hi heather,
here are the review questions
page 24 1,5,6
page 34 1-6 8-14
page 38 3-5

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 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.

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.


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.


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A crescent-shaped dimeric protein domain that binds membranes with its curved surface and thereby either senses membrane curvature or bends the membrane.

In-plane force counteracting membrane surface expansion.

Energy required to deform an elastic material. For lipid membranes, it contains a term for bending and a term for stretching, both taking the form of the energy associated with a harmonic spring: a constant called the modulus or rigidity, multiplied by the shape change to the square. Thus, bending energy is the bending rigidity multiplied by membrane curvature to the square, whereas stretching energy is the compressibility modulus multiplied by the area difference to the square. The elastic energy of the membrane is the sum of these two terms.

A short polypeptide, typically between 10 and 20 amino acids in length, that contains hydrophobic and hydrophilic residues. This polypeptide spontaneously folds into an α-helix when binding to a lipid membrane. In this configuration, all hydrophobic residues are aligned on the cylindrical face of the helix that is buried in the bilayer whereas the hydrophilic moieties are aligned on the hydrated face.

Fluorescence recovery after photobleaching

(FRAP). Microscopy method for measuring local exchange of fluorescently labelled molecules.

A highly conserved subfamily of monomeric myosin motors involved in cell motility and membrane traffic.

Forces that arise while the system tries to maximize its entropy. These forces typically arise from frustrated thermal fluctuations, which will then counteract the constraints by applying forces onto them. The pressure of an ideal gas is an entropic force. In lipid membranes, repulsive forces between closely apposed bilayers (less than a few tens of nanometres) — known as Helfrich forces — are entropic forces. They arise from thermal undulations of the bilayer surface. In polymer physics, thermal fluctuations usually lead to the folding of the polymer molecule into globular conformations. If one pulls on both ends of the molecule, an entropic force is felt.

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