Biology Reference
In-Depth Information
by a Ca
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-free proteolysis step that destroys cadherins (but that might also, caution requires
us to note, have destroyed other things too).
Taken at face value, this result provides good supporting evidence for the differential
adhesion model. Cells do express different adhesion molecules; they do spontaneously
sort as the model would predict, and the differently expressed adhesion molecules are neces-
sary for the sorting phenomenon to take place. This conclusion involves an assumption,
however, that different types of cadherin adhere to one another significantly less well than
they do to their own kind. There seem to have been no direct measurements of the relative
binding affinities of cadherins 4 and 6, but measurements have been made of other cadherin
pairs. Beads coated with cadherin 1, cadherin 2 or cadherin 3 adhere well to one another, with
broadly similar adhesion strengths whether the interaction was homophilic or heterophilic.
What is more, even the small differences that were seen were not consistently in favour of
homophilic interactions.
15
These conclusions based on coated beads have been confirmed
using atomic force microscopy that used a cantilever coated with a probe cadherin over
a plate coated with the sample cadherin.
16
The results of direct adhesion measurements do not predict the sorting behaviour of cells
expressing cadherins 1, 2 or 3
15,16
and, by extension, it seems unlikely that the sorting behav-
iour of neurepithelial cells expressing cadherins 4 and 6 will be explicable by the differential
adhesion model either. Something else, something more biological than simple thermo-
dynamics of adhesion, may be involved instead.
TH
EORY 2: BOUNDARY FORMATION BY TENSIO
N
One feature of compartment boundaries, especially obvious in
D. melanogaster
wing discs
and segments, is the presence of thick actin-myosin cables running along boundaries. Muta-
tions in, or RNAi-mediated knockdown of,
zipper
(the fly's non-muscle myosin II) result in
these cables not forming and in compartment boundaries becoming rough and irregular
rather than smooth and straight, suggesting cells from one compartment were able to invade
space that should have been the sole preserve of the other (
Figure 21.4
). The implication of
this observation is that tense actomyosin fibres are important to forming or maintaining
the boundary.
17
Tension could contribute to boundary function by at least three mechanisms. One is simple
suppression of motility: the antagonism between actomyosin stress fibres and assembly of
leading edge-type, motile actin structures has already been described in Chapter 9. Any
edge of a cell that is rich in stress fibres is unlikely to advance. Another result of tension is
boundary shortening: in the way that a slack rope can take on any shape but a tense one
will be straight, so a tense boundary should take up a shape as close to a straight line as other
forces (for example, cell compression) allow. Since cells can move within a compartment to
relieve these other forces, a straight boundary should eventually result. Third, within each
cell, the tensile forces running along the border side of the cell will 'try' to minimize the
area of the cell that faces that border. If a cell from the 'red' compartment starts to push
between cells of the 'blue' compartment, the tension in each type of cell will try to shorten
the new boundary that is created by the advance, and all will work together to restore
a smooth boundary (
Figure 21.5
). It is important to note a key difference between the system
