Chapter 9 Homeostasis And The Plasma Membrane Worksheet Answers.zip

Specialized cell junctions occur at points of cell-cell and cell-matrix contact in all tissues, and they are particularly plentiful in epithelia. Cell junctions are best visualized using either conventional or freeze-fracture electron microscopy (discussed in Chapter 9), which reveals that the interacting plasma membranes (and often the underlying cytoplasm and the intervening intercellular space as well) are highly specialized in these regions.

The tight junctions between epithelial cells are thought to have both of these roles. First, they function as barriers to the diffusion of some membrane proteins (and lipids) between apical and basolateral domains of the plasma membrane (see Figure 19-2). Mixing of such proteins and lipids occurs if tight junctions are disrupted, for example, by removing the extracellular Ca2+ that is required for tight junction integrity. Second, tight junctions seal neighboring cells together so that, if a low-molecular-weight tracer is added to one side of an epithelium, it will generally not pass beyond the tight junction (Figure 19-3). This seal is not absolute, however. Although all tight junctions are impermeable to macromolecules, their permeability to small molecules varies greatly in different epithelia. Tight junctions in the epithelium lining the small intestine, for example, are 10,000 times more permeable to inorganic ions, such as Na+, than the tight junctions in the epithelium lining the urinary bladder. These differences reflect differences in tight junction proteins that form the junctions.

When tight junctions are visualized by freeze-fracture electron microscopy, they seem to be composed of a branching network of sealing strands that completely encircles the apical end of each cell in the epithelial sheet (Figure 19-4A and B). In conventional electron micrographs, the outer leaflets of the two interacting plasma membranes are seen to be tightly apposed where sealing strands are present (Figure 19-4C). The ability of tight junctions to restrict the passage of ions through the spaces between cells is found to increase logarithmically with increasing numbers of strands in the network, suggesting that each strand acts as an independent barrier to ion flow.

Each tight junction sealing strand is composed of a long row of transmembrane adhesion proteins embedded in each of the two interacting plasma membranes. The extracellular domains of these proteins join directly to one another to occlude the intercellular space (Figure 19-5). The major transmembrane proteins in a tight junction are the claudins, which are essential for tight junction formation and function and differ in different tight junctions. A specific claudin found in kidney epithelial cells, for example, is required for Mg2+ to be resorbed from the urine into the blood. A mutation in the gene encoding this claudin results in excessive loss of Mg2+ in the urine. A second major transmembrane protein in tight junctions is occludin, the function of which is uncertain. Claudins and occludins associate with intracellular peripheral membrane proteins called ZO proteins (a tight junction is also known as a zonula occludens), which anchor the strands to the actin cytoskeleton.

In addition to claudins, occludins, and ZO proteins, several other proteins can be found associated with tight junctions. These include some that regulate epithelial cell polarity and others that help guide the delivery of components to the appropriate domain of the plasma membrane. Thus, the tight junction may serve as a regulatory center to help in coordinating multiple cell processes.

In invertebrates, septate junctions are the main occluding junction. More regular in structure than a tight junction, they likewise form a continuous band around each epithelial cell. But their morphology is distinct because the interacting plasma membranes are joined by proteins that are arranged in parallel rows with a regular periodicity (Figure 19-6). A protein called Discs-large, which is required for the formation of septate junctions in Drosophila, is structurally related to the ZO proteins found in vertebrate tight junctions. Mutant flies that are deficient in this protein not only lack septate junctions but also develop epithelial tumors. This observation suggests that the normal regulation of cell proliferation in epithelial tissues may depend, in part, on intracellular signals that emanate from occluding junctions.

Anchoring junctions are widely distributed in animal tissues and are most abundant in tissues that are subjected to severe mechanical stress, such as heart, muscle, and epidermis. They are composed of two main classes of proteins (Figure 19-8). Intracellular anchor proteins form a distinct plaque on the cytoplasmic face of the plasma membrane and connect the junctional complex to either actin filaments or intermediate filaments. Transmembrane adhesion proteins have a cytoplasmic tail that binds to one or more intracellular anchor proteins and an extracellular domain that interacts with either the extracellular matrix or the extracellular domains of specific transmembrane adhesion proteins on another cell. In addition to anchor proteins and adhesion proteins, many anchoring junctions contain intracellular signaling proteins that enable the junctions to signal to the cell interior.

Adherens junctions occur in various forms. In many nonepithelial tissues, they take the form of small punctate or streaklike attachments that indirectly connect the cortical actin filaments beneath the plasma membranes of two interacting cells. But the prototypical examples of adherens junctions occur in epithelia, where they often form a continuous adhesion belt (or zonula adherens) just below the tight junctions, encircling each of the interacting cells in the sheet. The adhesion belts are directly apposed in adjacent epithelial cells, with the interacting plasma membranes held together by the cadherins that serve here as transmembrane adhesion proteins.

The general structure of a desmosome is illustrated in Figure 19-11C, and some of the proteins that form it are shown in Figure 19-11D. The junction has a dense cytoplasmic plaque composed of a complex of intracellular anchor proteins (plakoglobin and desmoplakin) that are responsible for connecting the cytoskeleton to the transmembrane adhesion proteins. These adhesion proteins (desmoglein and desmocollin), like those at an adherens junction, belong to the cadherin family. They interact through their extracellular domains to hold the adjacent plasma membranes together.

Although the terminology for the various anchoring junctions can be confusing, the molecular principles (for vertebrates, at least) are relatively simple (Table 19-2). Integrins in the plasma membrane anchor a cell to extracellular matrix molecules; cadherin family members in the plasma membrane anchor it to the plasma membrane of an adjacent cell. In both cases, there is an intracellular coupling to cytoskeletal filaments, either actin filaments or intermediate filaments, depending on the types of intracellular anchor proteins involved.

The purpose of the pH regulation of gap-junction permeability is unknown. In one case, however, the purpose of Ca2+ control seems clear. When a cell is damaged, its plasma membrane can become leaky. Ions present at high concentration in the extracellular fluid, such as Ca2+ and Na+, then move into the cell, and valuable metabolites leak out. If the cell were to remain coupled to its healthy neighbors, these too would suffer a dangerous disturbance of their internal chemistry. But the large influx of Ca2+ into the damaged cell causes its gap-junction channels to close immediately, effectively isolating the cell and preventing the damage from spreading to other cells.

Running through the center of the channel in most plasmodesmata is a narrower cylindrical structure, the desmotubule, which is continuous with elements of the smooth endoplasmic reticulum in each of the connected cells (Figures 19-20B and 19-21A and B). Between the outside of the desmotubule and the inner face of the cylindrical channel formed by plasma membrane is an annulus of cytosol through which small molecules can pass from cell to cell. As each new cell wall is assembled during the cytokinesis phase of cell division, plasmadesmata are created within it. They form around elements of smooth ER that become trapped across the developing cell plate (discussed in Chapter 18). They can also be inserted de novo through pre-existing cell walls, where they are commonly found in dense clusters called pit fields (Figure 19-21C). When no longer required, plasmadesmata can be readily removed.

Many cells in tissues are linked to one another and to the extracellular matrix at specialized contact sites called cell junctions. Cell junctions fall into three functional classes: occluding junctions, anchoring junctions, and communicating junctions. Tight junctions are occluding junctions that are crucial in maintaining the concentration differences of small hydrophilic molecules across epithelial cell sheets. They do so in two ways. First, they seal the plasma membranes of adjacent cells together to create a continuous impermeable, or semipermeable, barrier to diffusion across the cell sheet. Second, they act as barriers in the lipid bilayer to restrict the diffusion of membrane transport proteins between the apical and the basolateral domains of the plasma membrane in each epithelial cell. Septate junctions serve as occluding junctions in invertebrate tissues.

The neurotransmitters of the ANS and the circulating catecholamines bind to specific receptors on the cell membranes of the effector tissue. All adrenergic receptors and muscarinic receptors are coupled to G proteins which are also embedded within the plasma membrane. Receptor stimulation causes activation of the G protein and the formation of an intracellular chemical, the second messenger. (The neurotransmitter molecule, which cannot enter the cell itself, is the first messenger.) The function of the intracellular second messenger molecules is to elicit tissue-specific biochemical events within the cell which alter the cell's activity. In this way, a given neurotransmitter may stimulate the same type of receptor on 2 different types of tissue and cause 2 different responses due to the presence of different biochemical pathways within each tissue. 2b1af7f3a8

Chapter 9 Homeostasis And The Plasma Membrane Worksheet Answers.zip

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