* I would like to remind the reader that a summary of these principles
can be found in Appendix I.
X
EVOLUTION:
THEME AND VARIATIONS
I refuse to believe that God plays dice with the world.
Albert Einstein
In the last chapter we were concerned with ontogeny -- the development
of the individual. We can now turn to phylogeny, and the crucial problem
of evolutionary progress.
The orthodox ('neo-Darwinian' or 'synthetic') theory attempts to explain
all evolutionary changes by random mutations (and re-combinations) of
genes; most mutations are harmful, but a very small proportion happens
to be useful and is retained by natural selection. As already mentioned,
'randomness' means in this context that the hereditary changes wrought
by mutation are totally unrelated to the animal's adaptive needs --
that they may alter its physique and behaviour 'in any and every direction.'
In this view, evolution appears as a game of blind man's buff. Or, in the
words of Professor Waddington -- a quasi-Trotskyite member of the
Establishment whom I shall have occasion to quote repeatedly in this
chapter: 'To suppose that the evolution of the wonderfully adapted
biological mechanisms has depended only on a selection out of a haphazard
set of variations, each produced by blind chance, is like suggesting that
if we went on throwing bricks together into heaps, we should eventually
be able to choose ourselves the most desirable house.' [1]
To illustrate the point, here is a simple example. The giant panda --
mascot of the World Wildlife Fund -- has on its forelimbs an added sixth
finger, which comes in very 'handy' for manipulating the bamboo-shoots
which are its principal food. But that added finger would be a useless
appendage without the proper muscles and nerves. The chances that among
all possible mutations those which produced the additional bones, muscles
and nerves should have occurred independently in the same population
are of course infinitesimally small. And yet in this case there are only
three variable factors involved. If we have, say, twenty factors (which
is still a modest estimate for the evolution of a complex organ), the
odds against their simultaneous alteration by chance alone become absurd,
and instead of scientific explanations, we should be trading in miracles.
Let us look at a less primitive example. The vertebrates' conquest of
dry land started with the evolution of reptiles from some primitive
amphibian form. The amphibians reproduced in the water, and their young
were aquatic. The decisive novelty of the reptiles was that, unlike
amphibians, they laid their eggs on dry land; they no longer depended
on the water and were free to roam over the continents. But the unborn
reptile inside the egg still needed an aquatic environment: it had
to have water or else it would dry up long before it was born. It also
needed a lot of food: amphibians hatch as larvae who fend for themselves,
whereas reptiles hatch fully developed. So the reptilian egg had to be
provided with a large mass of yolk for food, and also with albumen --
the white of egg -- to provide the water. Neither the yolk by itself,
nor the egg-white itself, would have had any selective value. Moreover,
the egg-white needed a vessel to contain it, otherwise its moisture would
have evaporated. So there had to be a shell made of a leathery or limey
material, as part of the evolutionary package-deal. But that is not the
end of the story. The reptilian embryo, because of this shell, could not
get rid of its waste products. The soft-shelled amphibian embryo had the
whole pond as a lavatory; the reptilian embryo had to be provided with
a kind of bladder. It is called the allantois, and is in some respects
the forerunner of the mammalian placenta. But this problem having been
solved, the embryo would still remain trapped inside its tough shell;
it needed a tool to get out. The embryos of some fishes and amphibians,
whose eggs are surrounded by a gelatinous membrane, have glands on their
snouts: when the time is ripe, they secrete a chemical which dissolves
the membrane. But embryos surrounded by a hard shell need a mechanical
tool: thus snakes and lizards have a tooth transformed into a kind of
tin-opener, while birds have a caruncle -- a hard outgrowth near the
tip of their beaks which serves the same purpose. In some birds --
the honey-guides -- which lay their eggs like cuckoos in alien nests,
the caruncle serves yet another purpose: it grows into a sharp hook
with which the newly hatched invader kills off his foster-brethren,
after which it amiably sheds the hook.
All this refers to one aspect only of the evolution of reptiles;
needless to say, countless other essential transformations of structure
and behaviour were required to make the new creatures viable. The changes
could have been gradual but at each step, however small,
all
the factors involved in the story had to co-operate harmoniously. The
liquid store in the egg makes no sense without the shell. The shell would
be useless, in fact murderous, without the allantois and without the
tin-opener. Each change, taken in isolation, would be harmful, and work
against
survival. You cannot have a mutation A occurring alone,
preserve it by natural selection, and then wait a few thousand or million
years until mutation B joins it, and so on, to C and D. Each mutation
occurring alone would be wiped out before it could be combined with the
others. They are all interdependent. The doctrine that their coming
together was due to a series of blind coincidences is an affront not
only to commonsense but to the basic principles of scientific explanation.
The propounders of the orthodox theory may have been uneasily aware
that something essential was missing, and paid occasional lip service
to 'unsolved problems', then hurriedly swept them under the carpet. To
quote one authority, Sir Peter Medawar (himself not excessively given
to tolerance of other people's opinions): 'Twenty years ago it all
seemed easy: with mutation as a source of diversity, with selection to
pick and choose. . . . Our former complacency can be traced, I suppose,
to an understandable fault of temperament: scientists tend not to ask
themselves questions until they can see the rudiments of an answer in
their minds. Embarrassing questions tend to remain unasked or, if asked,
to be answered rudely. . . . ' [1a]*
* Compare this with Sir Julian Huxley's ex cathedra pronouncement:
'In the field of evolution, genetics has given its basic answer,
and evolutionary biologists are free to pursue other problems.' [2]
A convenient way to evade these embarrassing questions was to concentrate
attention on the statistical treatment of mutations in large populations
of the fruit fly, Drosophila melanogaster -- the pet animal of geneticists
because it propagates so fast and has only four pairs of chromosomes. The
method is based on the measurement of the variations of some isolated,
and mostly trivial, characteristic, such as the colour of the eyes or
the distribution of bristles on the fly's body. Steeped in the atomistic
tradition, the upholders of the theory were apparently unable to see that
these mutations of a single factor -- virtually all of them deleterious
-- were quite irrelevant to the central problem of evolutionary progress,
requiring simultaneous changes in all the factors affecting the structure
and function of a complex organ. The geneticist's obsession with the
bristles of the fruit fly, and the Behaviourist's obsession with the
bar-pressing of the rat, show a more than superficial analogy. Both
derive from a mechanistic philosophy which regards the living creature
as a collection of elementary bits of behaviour (S-R units) and of
elementary bits of heredity (Mendelian genes).
Internal Selection
The alternative proposed here is the concept of the open hierarchy. Let
us see whether it can be applied to the evolutionary process. I shall
start by quoting Waddington's answer to problems of the type posed by
the giant panda's finger:
There are still some of us for whom the orthodox modern explanations
do not seem very satisfying. One well-known problem is this: many
organs are very complex things, and in order to bring about any
improvement in their functioning, it would be necessary to make
simultaneous alterations in several different characters . . . and
that, it might appear, is something which one would not expect to
occur under the influence of chance alone.
There have always been, and still are, reputable biologists who feel
that such considerations make it doubtful whether random hereditary
changes can provide a sufficient basis for evolution. But I believe
that the difficulty largely disappears if one remembers that an
organ like an eye is not simply a collection of elements, such as
a retina, a lens, an iris, and so on, which are put together and
happen to fit. It is something which is gradually formed while the
adult animal is developing out of the egg; and as the eye forms,
the different parts influence one another. Several people have
shown that if, by some experimental means, the retina and eyeball
are made larger than usual, that in itself will cause a larger
lens to appear, of at least approximately the appropriate size for
vision. There is no reason, therefore, why a chance mutation should
not affect the whole organ in a harmonious way; and there is
a reasonable possibility that it might improve it. . . . A random
change in a hereditary factor will, in fact, not usually result in
an alteration in just one element of the adult animal; it will bring
about a shift in the whole developmental system, and may thus alter
a complex organ as a whole. [3] (my italics)
We remember from the previous chapter that the growing eye-bud of the
embryo is an autonomous holon, which, if part of its tissue is taken away,
will nevertheless develop into a normal eye, thanks to its self-regulating
properties. It is by no means surprising that it should display the
same self-regulating powers, or 'flexible strategies' of growth, if the
disturbance is caused not by a human agent, but by a mutated gene, as
Waddington suggests. The chance mutation merely triggers off the process;
the 'prenatal skills' of the embryo will do the rest, in every successive
generation. The enlarged eye has become an evolutionary novelty.*
* It should be added that the example of the enlarged mutant eye is
typical of the sort of thing a mutating gene will do. Genes regulate
chemical reaction rates, including the rates of growth; and one of
the most frequent effects of gene mutations is to alter the speed
of growth of one part relative to others, and thus to modify the
proportions of the organ.
But embryonic development is a many-levelled hierarchic process; and
this leads one to assume that selective and regulative controls
operate on several levels to
eliminate
harmful mutations and to
co-ordinate
the effects of acceptable ones. Various authors*
have suggested that this screening process might start at the very
base of the hierarchy, on the level of the molecular chemistry of the
gene-complex. Mutations are chemical changes, presumably caused by the
impact of cosmic radiations and other factors, on the germ cells. The
changes consist in alterations in the sequence of the chemical units
in the chromosomes -- the four letters of the genetic alphabet. Mostly
they are the equivalents of misprints. But there seems to be again a
hierarchy of correctors and proof-readers at work to eliminate these;
'The struggle for survival of mutations begins at the moment mutation
occurs', writes L.L. Whyte. 'It is obvious that entirely arbitrary changes
will not be physically, chemically or functionally stable. . . . Only
those changes which result in a mutated system that satisfies certain
stringent physical, chemical and functional conditions will be able
to survive. . . . ' [4] All others will be eliminated, either by the
death of the mutated cell and its offspring at an early stage or, as we
shall presently see, by the remarkable self-repairing properties of the
gene-complex as a whole.
* Von Bertalanffy, Darlington, Spurway, Lima da Faria, L.L. Whyte.
See footnote on p. 147.
In the orthodox theory, natural selection is entirely due to the pressures
of the environment, which kills off the unfit and blesses the fit with
abundant progeny. In the light of the preceding considerations, however,
before a new mutation has a chance to be submitted to the Darwinian tests
of survival in the external environment, it must have passed the tests
of
internal selection
for its physical, chemical and biological fitness.
The concept of internal selection, of a hierarchy of controls which
eliminate the consequences of harmful gene-mutations and co-ordinates
the effects of useful mutations, is the missing link in orthodox
theory between the 'atoms' of heredity and the living stream of
evolution. Without that link, neither of them makes sense. There can
be no doubt that random mutations do occur: they can be observed in the
laboratory. There can be no doubt that Darwinian selection is a powerful
force. But in between these two events, between the chemical changes in
a gene and the appearance of the finished product as a newcomer on the
evolutionary stage, there is a whole hierarchy of internal processes at
work which impose strict limitations on the range of possible mutations
and thus considerably reduce the importance of the chance factor. We
might say that the monkey works at a typewriter which the manufacturers
have programmed to print only syllables which exist in our language,
but not nonsense syllables. If a nonsense syllable occurs, the machine
will automatically erase it.* To pursue the metaphor, we would have to
populate the higher levels of the hierarchy with proof-readers and then
editors, whose task is no longer elimination, but correction, self-repair
and co-ordination -- as in the example of the mutated eye.