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fold, die and do other things in response to the signals they perceive from their surroundings.
These signals provide feedback that controls the next step. In the glomerulus example, devel-
oping glomeruli secrete vascular endothelial growth factor (VEGF) and vascular cells migrate
towards it, stopping only when they detect that they have reached a glomerulus. 16 It does not
matter, therefore, if the glomeruli are in unexpected places due to errors in development; they
will be found automatically. This point is not just about kidneys; it is general. Another
example, described in detail in Chapter 24, is use of trophic feedback to match the number
of motor neurons to the number of their target muscle cells.
The power of feedback to confer robustness on a system applies not only to embryonic
timescales but also to the timescales of evolution. Within limits, an 'error' of construction
of one part of body plan, something that may be a useful evolutionary innovation, will be
accommodated automatically by the other systems on which it depends. A larger limb, for
example, will still receive enough innervation; a larger kidney will still receive enough
glomerular capillaries. Not all changes can be accommodated, but the number that can
greatly increases the probability of successful innovation. Such innovation can be triggered
by mutations that affect one body part without the necessity for a whole set of extra
mutations d a set whose simultaneous occurrence would be highly improbable d that simul-
taneously change the parts on which it depends.
There is an intriguing correlation between another specific aspect of robustness d
resistance to neoplastic disease d and the evolutionary age of an organ. This is linked to
morphogenesis because neoplastic disease arises from inappropriate activation of morphoge-
netic processes such as proliferation and migration. In humans, at least, cancer rates are
much lower in internal organs that are present even in basal vertebrates and highest in organs
such as prostate and mammary glands that have arisen most recently, middle-aged organs
having middling rates of cancer. 17 It is not immediately obvious why this should be the
case. Neoplasia arises so late in life, compared with reproduction, that gradual selection
for mechanisms of resistance to it is unlikely to have been a major cause of this correlation.
Perhaps the pattern instead reflects greater fragility of new developmental sequences that
have added yet more stages to already complicated development. If it does, it may indicate
that there will be a limit to how many times new developmental mechanisms can co-opt
existing ones, that in turn had co-opted older ones, and so on.
The Useful-Yet-Dangerous Metaphor of Modularity
When seeking a word to describe the lower-level systems that are grouped to produce
higher level ones d that are in turn grouped d the word 'module' springs naturally to
mind. By analogy with engineering, each level consists of a 'module' that can be called by
higher level processes in the developmental programme, which will themselves form
a module of another level. In some contexts, the self-assembly of a single macromolecular
complex may be treated as a module, whereas in other contexts the assembly of a leading
edge, or perhaps of a whole population of migrating cells, may be considered as a module.
The language is very helpful in providing an easy way to discuss the many-layered organ-
ization of morphogenetic mechanisms, and the concept of a module is a very useful aid in
the interpretation of whole-genome microarray studies of tissues that are undergoing
a morphogenetic event. Indeed, this language was evoked and used (with a warning) in
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