Molecular Biology of the Cell by Bruce Alberts, Alexander Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter by by Bruce Alberts, Alexander Johnson, Julian Lewis, David Morg

THE PLANT CELL WALL
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In this way, plant cells can change their direction of expansion by a sudden
change in the orientation of their cortical array of microtubules. Because plant
cells cannot move (being constrained by their walls), the entire morphology of
a multicellular plant presumably depends on a coordinated, highly patterned
deployment of cortical microtubule orientations during plant development. It is
not known how these orientations are controlled, although it has been shown that
the microtubules can reorient rapidly in response to extracellular stimuli, including
plant growth regulators such as ethylene and auxins (discussed in Chapter 15).
Microtubules are not, however, the only cytoskeletal elements that influence
wall deposition. Local foci of cortical actin filaments can also direct the deposition
of new wall material at specific sites on the cell surface, contributing to the elaborate
final shaping of many differentiated plant cells.
Summary
Plant cells are surrounded by a tough extracellular matrix, or cell wall, which is
responsible for many of the unique features of a plant’s lifestyle. The wall is composed
of a network of cellulose microfibrils and cross-linking glycans, embedded in
a highly cross-linked matrix of pectin polysaccharides. In secondary cell walls, lignin
may be deposited to make them waterproof, hard, and woody. A cortical array
of microtubules can control the orientation of newly deposited cellulose microfibrils,
which in turn determine the direction of cell expansion and therefore the final
shape of the cell and, ultimately, of the plant as a whole.
Problems
Which statements are true? Explain why or why not.
19–1 Given the numerous processes inside cells that
are regulated by changes in Ca 2+ concentration, it seems
likely that Ca 2+ -dependent cell–cell adhesions are also
regulated by changes in Ca 2+ 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
proteins.
19–3 The elasticity of elastin derives from its high content
of α helices, which act as molecular springs.
19–4 Integrins can convert mechanical signals into
intracellular molecular signals.
Discuss the following problems.
19–5 Comment on the following (1922) quote from
Warren Lewis, who was one of the pioneers of cell biology.
“Were the various types of cells to lose their stickiness for
one another and for the supporting extracellular matrix,
our bodies would at once disintegrate and flow off into the
ground in a mixed stream of cells.”
19–6 Cell adhesion molecules were originally identified
using antibodies raised against cell-surface components
to block cell aggregation. In the adhesion-blocking
assays, the researchers found it necessary to use antibody
fragments, each with a single binding site (so-called Fab
fragments), rather than intact IgG antibodies, which are
Y-shaped molecules with two identical binding sites. The
sites of
papain
cleavage
IgG antibody
What we don’t know
• What are the regulatory mechanisms
that control the rearrangement of
cell–cell junctions in epithelia during
early development? What roles do
mechanical force and tension play in
these rearrangements?
• How do extracellular matrix proteins
and carbohydrates influence the
localization and actions of extracellular
signal molecules or their cell-surface
receptors?
• How do intracellular adaptor proteins
coordinate the activation of integrin
proteins and their interactions with
cytoskeletal components and their
response to changes in mechanical
force acting on cell–matrix junctions?
• Given that extracellular matrix
molecules have the ability to present
ordered arrays of signals to cells,
might the exact spatial relationships
between such signals carry a message
beyond that of the individual signals
themselves?
PAPAIN
sites for
antigen binding
Fab fragments
Figure Q19–1 Production of Fab fragments from IgG antibodies by
digestion with papain (Problem 19–6).
Fab fragments were generated by digesting the IgG antibodies
with papain, a protease, to separate the two binding
sites (Figure Q19–1). Why do you suppose it was necessary
to use Fab fragments to block cell aggregation?
Problems p19.01/19.01
19–7 The food-poisoning bacterium Clostridium perfringens
makes a toxin that binds to members of the claudin
family of proteins, which are the main constituents of
tight junctions. When the C-terminus of the toxin is bound
to a claudin, the N-terminus can insert into the adjacent
cell membrane, forming holes that kill the cell. The portion
of the toxin that binds to the claudins has proven to be
a valuable reagent for investigating the properties of tight
junctions. MDCK cells are a common choice for studies
of tight junctions because they can form an intact epithelial
sheet with high transepithelial resistance. MDCK cells
express two claudins: claudin-1, which is not bound by
the toxin, and claudin-4, which is.
When an intact MDCK epithelial sheet is incubated
with the C-terminal toxin fragment, claudin-4
disappears, becoming undetectable within 24 hours. In