coordinate the activation of integrin Plant cells are surrounded by a tough extracellular matrix, or cell wall, which is proteins and their interactions with responsible for many of the unique features of a plant’s lifestyle. The wall is com-cytoskeletal components and their posed of a network of cellulose microfibrils and cross-linking glycans, embedded in response to changes in mechanical a highly cross-linked matrix of pectin polysaccharides. In secondary cell walls, lig-force acting on cell–matrix junctions? nin may be deposited to make them waterproof, hard, and woody. A cortical array of microtubules can control the orientation of newly deposited cellulose microfi molecules have the ability to present brils, which in turn determine the direction of cell expansion and therefore the final ordered arrays of signals to cells, shape of the cell and, ultimately, of the plant as a whole. might the exact spatial relationships between such signals carry a message beyond that of the individual signals themselves?
Which statements are true? explain why or why not. sites of sites for 19–1 Given the numerous processes inside cells that cleavage are regulated by changes in Ca2+ concentration, it seems likely that Ca2+-dependent cell–cell adhesions are also regulated by changes in Ca2+ concentration.
19–2 Tight junctions perform two distinct functions: they seal the space between cells to restrict paracellular flow and they fence off plasma membrane domains to prevent the mixing of apical and basolateral membrane Figure Q19–1 Production of Fab fragments from IgG antibodies by digestion with papain (problem 19–6).
proteins.
19–3 The elasticity of elastin derives from its high con-Fab fragments were generated by digesting the IgG anti-tent of α helices, which act as molecular springs. bodies with papain, a protease, to separate the two binding sites (Figure Q19–1). Why do you suppose it was nec19–4 Integrins can convert mechanical signals into essary to use Fab fragments to block cell aggregation? intracellular molecular signals. 19–7 The food-poisoning bacterium Clostridium per-Discuss the following problems. fringens makes a toxin that binds to members of the claudin family of proteins, which are the main constituents of 19–5 Comment on the following (1922) quote from tight junctions. When the C-terminus of the toxin is bound Warren Lewis, who was one of the pioneers of cell biology.
to a claudin, the N-terminus can insert into the adjacent “Were the various types of cells to lose their stickiness for cell membrane, forming holes that kill the cell. The porone another and for the supporting extracellular matrix, tion of the toxin that binds to the claudins has proven to be our bodies would at once disintegrate and flow off into the a valuable reagent for investigating the properties of tight ground in a mixed stream of cells.” junctions. MDCK cells are a common choice for studies 19–6 Cell adhesion molecules were originally identi-of tight junctions because they can form an intact epithefied using antibodies raised against cell-surface compo-lial sheet with high transepithelial resistance. MDCK cells nents to block cell aggregation. In the adhesion-blocking express two claudins: claudin-1, which is not bound by assays, the researchers found it necessary to use antibody the toxin, and claudin-4, which is. fragments, each with a single binding site (so-called Fab When an intact MDCK epithelial sheet is incufragments), rather than intact IgG antibodies, which are bated with the C-terminal toxin fragment, claudin-4 Y-shaped molecules with two identical binding sites. The disappears, becoming undetectable within 24 hours. In (A) BASOLATERAL (B) APICAL 10,000