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

CELL–CELL JUNCTIONS
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adhesion belt with
associated actin filaments
sheet of epithelial cells
INVAGINATION OF EPITHELIAL SHEET CAUSED
BY AN ORGANIZED TIGHTENING OF
ADHESION BELTS IN SELECTED REGIONS OF
CELL SHEET
Figure 19–14 The folding of an epithelial
sheet to form an epithelial tube. The
oriented contraction of the bundles of
actin and myosin filaments running along
adhesion belts causes the epithelial cells to
narrow at their apex and helps the epithelial
sheet to roll up into a tube. An example
is the formation of the neural tube in early
vertebrate development (see Figure 19–8).
EPITHELIAL TUBE PINCHES OFF
FROM OVERLYING SHEET OF CELLS
epithelial
tube
it by the cadherins and their associated intracellular adaptor proteins. The actin–
myosin bundles are thus linked, via the cadherins, into an extensive transcellular
network. Coordinated contraction of this network provides the motile force for
a fundamental process in animal morphogenesis—the folding of epithelial cell
sheets into tubes, vesicles, MBoC6 and other m19.16/19.14 related structures (Figure 19–14).
The coordination of cell–cell adhesion and actin contractility is beautifully
illustrated by cellular rearrangements that occur early in the development of the
fruit fly Drosophila melanogaster. Soon after gastrulation, the outer epithelium
of the embryo is elongated by a process called germ-band extension, in which the
cells converge inward toward the dorsal–ventral axis and extend along the anterior–posterior
axis (Figure 19–15). Actin-dependent contraction along specific
cell boundaries is coordinated with a loss of specific adherens junctions to allow
cells to insert themselves between other cells (a process called intercalation),
resulting in a longer and narrower epithelium. The mechanisms underlying the
loss of adhesion along specific cell boundaries are not clear, but they depend in
part on increased degradation of β-catenin, due to its phosphorylation by a protein
kinase that is localized specifically at those boundaries.
Desmosomes Give Epithelia Mechanical Strength
Desmosomes are structurally similar to adherens junctions but contain specialized
cadherins that link to intermediate filaments instead of actin filaments. Their
main function is to provide mechanical strength. Desmosomes are important
anterior
dorsal
ventral
posterior
actin–myosin
cadherin
Figure 19–15 Remodeling of cell–cell
adhesions in embryonic Drosophila
epithelium. Depicted at left is a group of
cells in the outer epithelium of a Drosophila
embryo. During germ-band extension, cells
converge toward each other (middle) on
the dorsal–ventral axis and then extend
(right) along the anterior–posterior axis.
The result is intercalation: cells that were
originally far apart along the dorsal–ventral
axis (dark green) are inserted between
the cells (light green) that separated
them. These rearrangements depend
on the spatial regulation of actin–myosin
contractile bundles, which are localized
primarily at the vertical cell boundaries
(red, left). Contraction of these bundles is
accompanied by removal of E-cadherin
(not shown) at the same cell boundaries,
resulting in shrinkage and loss of adhesion
along the vertical axis (middle). New
cadherin-based adhesions (blue, right)
then form and expand along horizontal
boundaries, resulting in extension of the
cells in the anterior–posterior dimension.