188
8 Morphogenesis
of remodeling. There are some speculations about the way precision is attained in
addressing and the way errors are dealt with. Misdirected cells may commit suicide,
through apoptosis, or may retrain for another job.
The mechanisms of cell rearrangement and sorting, their collective migration,
and folding of epithelial layers in the embryo do not differ in principle from those
discussed in Chap. 7, but they have to follow specific genetic cues, likely selfsustained by the cells involved. Thus, genetic mechanisms regulating intercalation in
Drosophila were uncovered by Irvine and Wieschaus (1994). This is an efficient tool
for tissue elongation (accompanied by lateral contraction), as illustrated in Fig. 8.17.
Stiffening was observed in collectively migrating cells (Barriga et al, 2018), which
may be a sign of a supracellular cytoskeletal organization between multiple cells
allowing them to function as a single unit. Yet, mechanics of cellular flow remains
poorly understood due to difficulties in measuring driving forces.
As noted in Sect. 7.1, intercalation, as well as mitosis, increases the disorder of a
cellular layer. In some organs, where a regular arrangement is essential, the hexagonal
tiling is restored at a later stage. The patterning of Drosophila’s wings is already
regularized on the adult stage, at the start of bristle growth (Classen et al, 2005),
and requires the rearrangement of intercellular junctions, also guided genetically.
Order is essential in retinal patterning. Insect’s eyes contain an ordered array of
hexagonal units called ommatidia. Their assembly is a complex process (Voas and
Rebay, 2004), where ordering is established by an autoregulatory feedback loop
between neighboring cells, disrupted by mutations.
Cell sorting serves to maintain boundaries between cell patches with different
fates. The most common mechanism is based on differential adhesion properties
(Sect. 7.1). Another model states that specific mechanical properties of cells at
the boundaries prevent cell mixing through the formation of a stiff barrier that
cells cannot cross. Both mechanisms are regulated genetically and are responsible
for surface tension that prevents the addition and stabilization of new cells at the
boundary and reduces the area of contact between compartments. The role of cell
Fig. 8.18 (a) Top: Time-lapse images of a cellular layer marking the constriction (C) and stabilization (S) phases of the cell marked by the red dot. Bottom: Color-coded constriction rates at
consecutive time moments. Scale bar 4 μm. (b) Left: Change in the mean apical area and myosin
intensity with time. Right: Color-coded myosin intensity of individual cells (Martin et al, 2009)
8 Morphogenesis
of remodeling. There are some speculations about the way precision is attained in
addressing and the way errors are dealt with. Misdirected cells may commit suicide,
through apoptosis, or may retrain for another job.
The mechanisms of cell rearrangement and sorting, their collective migration,
and folding of epithelial layers in the embryo do not differ in principle from those
discussed in Chap. 7, but they have to follow specific genetic cues, likely selfsustained by the cells involved. Thus, genetic mechanisms regulating intercalation in
Drosophila were uncovered by Irvine and Wieschaus (1994). This is an efficient tool
for tissue elongation (accompanied by lateral contraction), as illustrated in Fig. 8.17.
Stiffening was observed in collectively migrating cells (Barriga et al, 2018), which
may be a sign of a supracellular cytoskeletal organization between multiple cells
allowing them to function as a single unit. Yet, mechanics of cellular flow remains
poorly understood due to difficulties in measuring driving forces.
As noted in Sect. 7.1, intercalation, as well as mitosis, increases the disorder of a
cellular layer. In some organs, where a regular arrangement is essential, the hexagonal
tiling is restored at a later stage. The patterning of Drosophila’s wings is already
regularized on the adult stage, at the start of bristle growth (Classen et al, 2005),
and requires the rearrangement of intercellular junctions, also guided genetically.
Order is essential in retinal patterning. Insect’s eyes contain an ordered array of
hexagonal units called ommatidia. Their assembly is a complex process (Voas and
Rebay, 2004), where ordering is established by an autoregulatory feedback loop
between neighboring cells, disrupted by mutations.
Cell sorting serves to maintain boundaries between cell patches with different
fates. The most common mechanism is based on differential adhesion properties
(Sect. 7.1). Another model states that specific mechanical properties of cells at
the boundaries prevent cell mixing through the formation of a stiff barrier that
cells cannot cross. Both mechanisms are regulated genetically and are responsible
for surface tension that prevents the addition and stabilization of new cells at the
boundary and reduces the area of contact between compartments. The role of cell
Fig. 8.18 (a) Top: Time-lapse images of a cellular layer marking the constriction (C) and stabilization (S) phases of the cell marked by the red dot. Bottom: Color-coded constriction rates at
consecutive time moments. Scale bar 4 μm. (b) Left: Change in the mean apical area and myosin
intensity with time. Right: Color-coded myosin intensity of individual cells (Martin et al, 2009)