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7.13: Introduction to Endocytosis and Exocytosis - Biology

7.13: Introduction to Endocytosis and Exocytosis - Biology


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Describe the primary mechanisms by which cells import and export macromolecules

In addition to moving small ions and molecules through the membrane, cells also need to remove and take in larger molecules and particles. A large particle, however, cannot pass through the membrane, even with energy supplied by the cell.

There are two primary mechanisms that transport these large particles: endocytosis and exocytosis.

What You’ll Learn to Do

  • Describe endocytosis and identify different varieties of import, including phagocytosis, pinocytosis, and receptor-mediated endocytosis
  • Identify the steps of exocytosis

Learning Activities

The learning activities for this section include the following:

  • Endocytosis
  • Exocytosis
  • Self Check: Endocytosis and Exocytosis

Exocytosis and Endocytosis

Exocytosis: Membrane proteins are fine for channeling the movement of ions and small molecules, but for transporting large molecules, a different strategy is required. When cells need to send large molecules (like proteins) outside their plasma membrane borders, they turn to exocytosis. Sizable cargo is loaded into spherical membrane vesicles. These vesicles move toward the plasma membrane and fuse with it, exposing the vesicle interior to the outside of the cell and releasing its contents.

Endocytosis: Sometimes cells have cause to import large molecules. For this challenging task, the solution is endocytosis, which is essentially exocytosis in reverse. Molecules to be imported contact the exterior surface of the plasma membrane, triggering the membrane to fold inward, enveloping them. The infolded membrane pinches off into a vesicle containing the imported molecules, which can be further transported to their eventual destination within the cell.


REVIEW article

Kuo Liang 1 † , Lisi Wei 2 † and Liangyi Chen 2 *
  • 1 Department of General Surgery, XuanWu Hospital, Capital Medical University, Beijing, China
  • 2 State Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine, Peking University, Beijing, China

Evoked exocytosis in excitable cells is fast and spatially confined and must be followed by coupled endocytosis to enable sustained exocytosis while maintaining the balance of the vesicle pool and the plasma membrane. Various types of exocytosis and endocytosis exist in these excitable cells, as those has been found from different types of experiments conducted in different cell types. Correlating these diversified types of exocytosis and endocytosis is problematic. By providing an outline of different exocytosis and endocytosis processes and possible coupling mechanisms here, we emphasize that the endocytic pathway may be pre-determined at the time the vesicle chooses to fuse with the plasma membrane in one specific mode. Therefore, understanding the early intermediate stages of vesicle exocytosis may be instrumental in exploring the mechanism of tailing endocytosis.


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From the Back Cover

Due to their vital involvement in a wide variety of housekeeping and specialized cellular functions, exocytosis and endocytosis remain among the most popular subjects in biology and biomedical sciences. Tremendous progress in understanding these complex intracellular processes has been achieved by employing a wide array of research tools ranging from classical biochemical methods to modern imaging techniques. In Exocytosis and Endocytosis , skilled experts provide the most up-to-date,step-by-step laboratory protocols for examining molecular machinery and biological functions of exocytosis and endocytosis in vitro and in vivo . Following the highly successful Methods in Molecular Biology™ series format, the chapters present an introduction outlining the principle behind each technique, a list of the necessary materials, an easy to follow, readily reproducible protocol, and a Notes section offering tips on troubleshooting and avoiding known pitfalls.

Insightful to both newcomers and seasoned professionals, Exocytosis and Endocytosis offers a unique and highly practical guide to versatile laboratory tools developed to study various aspects of intracellular vesicle trafficking in simple model systems and living organisms.


Types of Exocytosis

Encyclopaedia Britannica / UIG / Getty Images

There are three common pathways of exocytosis. One pathway, constitutive exocytosis, involves the regular secretion of molecules. This action is performed by all cells. Constitutive exocytosis functions to deliver membrane proteins and lipids to the cell's surface and to expel substances to the cell's exterior.

Regulated exocytosis relies on the presence of extracellular signals for the expulsion of materials within vesicles. Regulated exocytosis occurs commonly in secretory cells and not in all cell types. Secretory cells store products such as hormones, neurotransmitters, and digestive enzymes that are released only when triggered by extracellular signals. Secretory vesicles are not incorporated into the cell membrane but fuse only long enough to release their contents. Once the delivery has been made, the vesicles reform and return to the cytoplasm.

A third pathway for exocytosis in cells involves the fusion of vesicles with lysosomes. These organelles contain acid hydrolase enzymes that break down waste materials, microbes, and cellular debris. Lysosomes carry their digested material to the cell membrane where they fuse with the membrane and release their contents into the extracellular matrix.


Dynamin and endocytosis inhibitors

Dynamin is a key GTPase involved in various forms of endocytosis and is comprised of 3 major isoforms, all of which have four main functional domains.

In addition to being a key component of endocytosis, dynamin participates in cell cycle progression and has also been shown to have critical roles in centrosome cohesion and cytokinesis.

Dynamin inhibitors inhibit different domains of dynamin, leading to subsequent inhibition of endocytosis. Consequently, the dynamin inhibitors have wide-spread application allowing investigation of cell signalling pathways, the cell cycle and cellular division, in addition to other medical conditions such as cancer, neurological conditions and infectious diseases such as botulism and HIV.

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Exocytosis and Endocytosis: Modes, Functions, and Coupling Mechanisms

Vesicle exocytosis releases content to mediate many biological events, including synaptic transmission essential for brain functions. Following exocytosis, endocytosis is initiated to retrieve exocytosed vesicles within seconds to minutes. Decades of studies in secretory cells reveal three exocytosis modes coupled to three endocytosis modes: (a) full-collapse fusion, in which vesicles collapse into the plasma membrane, followed by classical endocytosis involving membrane invagination and vesicle reformation (b) kiss-and-run, in which the fusion pore opens and closes and (c) compound exocytosis, which involves exocytosis of giant vesicles formed via vesicle-vesicle fusion, followed by bulk endocytosis that retrieves giant vesicles. Here we review these exo- and endocytosis modes and their roles in regulating quantal size and synaptic strength, generating synaptic plasticity, maintaining exocytosis, and clearing release sites for vesicle replenishment. Furthermore, we highlight recent progress in understanding how vesicle endocytosis is initiated and is thus coupled to exocytosis. The emerging model is that calcium influx via voltage-dependent calcium channels at the calcium microdomain triggers endocytosis and controls endocytosis rate calmodulin and synaptotagmin are the calcium sensors and the exocytosis machinery, including SNARE proteins (synaptobrevin, SNAP25, and syntaxin), is needed to coinitiate endocytosis, likely to control the amount of endocytosis.


1. INTRODUCTION

Cells respond to internal and external cues by selectively permitting growth in specific regions of the cell membrane to achieve non-spherical shapes [1]. Studies have found that the actin cytoskeleton, a major target of signaling events, undergoes rearrangement and mediates transport of proteins, organelles and secretory vesicles toward sites of growth, giving rise to polarized morphogenesis ([2, 3], reviewed in [4] and [5]).

In morphogenesis of yeast and mammalian cells, the organization of the actin cytoskeleton and vesicle transport along a vectorial axis requires an intricate regulation orchestrated by active G-proteins, Cdc42p and other GTPases, to control the establishment of polarity [3, 6, 7]. Activation of Cdc42p leads to a localized recruitment of actin cables and actin patches at the site of Cdc42p accumulation on the cell membrane however, the details of the pathways linking Cdc42p to actin polymerization are still unclear [8].

Since morphogenesis requires sustained assembly of actin cables, the maintenance of Cdc42p polarization and other cortical proteins is crucial. Three general schemes have been invoked to explain such polarization [4]: (1) a preexisting stably polarized 𠇊nchor” interacts with a protein of interest, thereby increasing its concentration for example, in yeast budding, 𠇋ud site selection” proteins are deposited at the cell poles during bud formation, allowing them to serve as “landmarks” that bind anchor proteins in subsequent cell cycles [9] (2) a diffusion barrier is established that prevents protein diffusion between compartments in budding yeast, septin filament systems act as a diffusion barrier during budding (3) dynamic control through polarized delivery and endocytic retrieval of cortical proteins to sites of polarization thereby limiting the length scale of lateral membrane diffusion. In yeast mating projection (shmoo) formation, a morphorgenesis process in which no evident diffusion barrier has been found (although the septin structure at the base of the projection may potentially act in this manner), endocytosis and exocytosis could play critical roles in both maintaining polarity and expanding the membrane to produce the projection, if the proteins and vesicles are kinetically recycled and fuse with the native membrane, leading to a change in the total area of cell membrane.

In experiments of S. cerevisiae exposed to differential mating pheromone concentrations, different cell morphologies were observed. At high pheromone concentrations, mating projections are observed to be thinner and shorter than those exposed to lower pheromone concentrations. Previous studies suggest that endocytosis is a receptor-mediated process where binding of extracellular ligand by the extracellular portion of transmembrane receptors facilitates heterotrimeric G-protein activation and internalization of the receptor-ligand complex [10], and exocytosis regulated by the intracellular signaling of Cdc42p [11]. This evidence leads us to propose that differential cell morphologies in response to ligand concentration are a result of the balance between endocytosis and exocytosis, in other words, a balance between G-protein and Cdc42p signaling.

An efficient way to test this hypothesis is to develop a mathematical model that incorporates the signaling transduction pathway and permits deformation of the cell membrane. A number of mathematical models have been developed to investigate dynamics of actin filaments in cell morphogenesis [12, 13]. Different aspects of actin dynamics, such as the actin monomer cycle and actin polymerization at the leading cell edge [14], and roles of vesicle trafficking on signaling and polarization [15, 16], are inspected in various models. Fluid-based models are also used to simulate the motion or deformation of eukaryotic cells [17-19]. Level set approaches coupled with the associated biochemistry are used to approximate the deforming cell membrane [20-22].

In this paper, we propose a mathematical model that couples the signaling pathway and the deforming cell membrane. We will first introduce a single-module model to demonstrate the capability of the model to generate budding and mating projections morphologies in yeast cells. Then we will explain the pheromone dependent experimental data by using a two-module model of Gβγ (G-protein) and Cdc42p signaling, whose levels correlate with levels of endocytosis and exocytosis. It is important to note that this division of labor between heterotrimeric G-protein and Cdc42 is a model hypothesis (and simplification) that needs to be tested and refined by further experiments. Nevertheless, numerical simulations show that different balances between Gβγ and Cdc42p signaling indeed result in differential cell length and width, and the cell morphologies are consistent with the experimental results both qualitatively and quantitatively.


Bulk Transport of Meterials Into and Out of Cells (With Diagram)

Before we consider several mechanisms responsible for bulk movement of materials into and out of cells, it is important that, what is meant by “inside the cell” and “outside the cell”.

The plasma mem­brane as a more or less continuous smooth sheet en- dosing the cell. In reality, this is an oversimplification, for in most cells the plasma membrane exhibits nu­merous outflings and inholdings.

Outfoldings of the plasma membrane cover microvilli, cilia, flagella, and other cytoplasmic extensions. Infoldings of the plasma membrane form small pockets and narrow channels that descend into the cytosol.

Some of these infoldings may join the network of cisternae that form the endoplasmic reticulum and that furrow the cyto­plasm.

This implies that the intracisternal space of the endoplasmic reticulum may be in direct continuity with the surrounding cell environment and that the movement of materials between the lumenal phase and the cell surroundings does not require passage across (or through) any membranes. Consequently, any materials that are in the cisternae of the endo­plasmic reticulum (i.e., in the lumenal phase) may be regarded as “outside” the cell. To get “inside” the cell, substances in the lumenal phase must pass through the membranous walls of the endoplasmic re­ticulum and into the cytosol.

Many intracellular vesicles appear to be derived from the endoplasmic reticulum by being “pinched off from the latter. For example, transitional vesi­cles that merge with the forming face of the cell’s Golgi bodies and peroxisomes and other micro bodies are believed to be formed in this way.

Technically then, the contents of these vesi­cles are “outside” the cell and are separated from the cytosol by membranes. Some vesicles are derived from invaginations of the plasma membrane the con­tents of these vesicles are also to be considered as “outside” the cell. These relationships are depicted in Figure 15-42, in which the external (or cisternal) and internal (or cytosol) halves of the membrane are distinguished. Particles within such a vesicle are in con­tact with the external face of the membrane.

From the preceding discussion, it should be clear that though substances may be directly exchanged be­tween the cell surroundings and the cytosol through the plasma membrane, many exchanges also occur across membranes of cytoplasmic vesicles and the en­doplasmic reticulum. These exchanges are mediated by the same mechanisms described above in connec­tion with movements directly through the plasma membrane (i.e., diffusion, facilitated diffusion, active transport, etc.).

The formation of cytoplasmic vesicles from the plasma membrane and the consequent entrapment within these vesicles of substances formerly in the cell surroundings is called endocytosis. Several different kinds of endocytosis have been described, including pinocytosis, phagocytosis, and receptor-mediated endocytosis.

Move­ments of materials from the cell into the surroundings by the fusion of cytoplasmic vesicles with the plasma membrane constitute exocytosis. Endocytosis contin­uously removes small portions of the plasma mem­brane, whereas exocytosis continuously adds to the membrane.


Exocytosis and Endocytosis: Modes, Functions, and Coupling Mechanisms

Vesicle exocytosis releases content to mediate many biological events, including synaptic transmission essential for brain functions. Following exocytosis, endocytosis is initiated to retrieve exocytosed vesicles within seconds to minutes. Decades of studies in secretory cells reveal three exocytosis modes coupled to three endocytosis modes: (a) full-collapse fusion, in which vesicles collapse into the plasma membrane, followed by classical endocytosis involving membrane invagination and vesicle reformation (b) kiss-and-run, in which the fusion pore opens and closes and (c) compound exocytosis, which involves exocytosis of giant vesicles formed via vesicle-vesicle fusion, followed by bulk endocytosis that retrieves giant vesicles. Here we review these exo- and endocytosis modes and their roles in regulating quantal size and synaptic strength, generating synaptic plasticity, maintaining exocytosis, and clearing release sites for vesicle replenishment. Furthermore, we highlight recent progress in understanding how vesicle endocytosis is initiated and is thus coupled to exocytosis. The emerging model is that calcium influx via voltage-dependent calcium channels at the calcium microdomain triggers endocytosis and controls endocytosis rate calmodulin and synaptotagmin are the calcium sensors and the exocytosis machinery, including SNARE proteins (synaptobrevin, SNAP25, and syntaxin), is needed to coinitiate endocytosis, likely to control the amount of endocytosis.


Watch the video: Cell Transport - Endocytosis, Exocytosis, Phagocytosis, and Pinocytosis (May 2022).


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