These pages have been left in this location as a service to the numerous websites around the world which link to this content. The original authors are no longer at the University of Leeds, and the former Centre for Human Biology became the School of Biomedical Sciences which is now part of the Faculty of Biological Sciences.
Phylogeny and ontogeny are very similar: the only difference
is that ontogeny goes along a very fixed path - a hens egg always
finishes up as a chicken, a mouse's egg always ends up as a mouse
but ontogeny, according to Darwin, is a random walk. There is
obviously a way of modifying phylogeny - does this mean that
there must be a way of changing ontogeny?
So, how do we start to study the problem? First of all what
are the differences between animals? In general the differences
are anatomical ones, differences in shape. The basic chemicals
involved are pretty much the same. Haemoglobin is found in annelid
worms and in vertebrates. The base sequence is very similar in
each case. Cytochrome, collagen, many molecules are widespread
and very similar at most critical points wherever they are found.
The basic fixings between cells (desmosomes, gap junctions) are
the same. Animals are largely made out of the same stuff, but
it is arranged differently. Anatomical differences arise anew
in each generation ( we have seen that the early larval forms
of many marine organisms are very similar, so much so that we
have to wait till they grow up to see if we have a mollusc or
a crab: early chick, mouse and human embryos are similar) and
also arose through time by evolution.
If Haeckel was right, and animals are all related we ought
to be able to make supergroups of phyla, using Bauplans. In fact
we can, but we can do this in different ways, because we don't
know the 'correct' rules for making these supergroups (OVERHEAD).
Some of the more sensible guesses are: (OVERHEAD)
1. Number of germ layers - diploblasts versus triploblasts
2. Type of symmetry - bilateral versus radial
3. Pattern of embryonic cleavage - some animals eggs divide spirally, some don't (OVERHEAD).
4. Development of the coelom - interior cavity (OVERHEAD)
5. Original opening forms mouth or anus (OVERHEAD)
6. ventral or dorsal nervous system (OVERHEAD)
All these are perfectly respectable, but we don't know which,
if any is valid. It is quite good fun playing this game. Nielson
(1995), as we have already mentioned, did to good effect and
has come up with a tree which explains most things, (OVERHEAD)
although five phyla (non of them very large) are problematical.
He starts off with the monophyletic phylum as a group and works
out relationships from there.
Basically, Nielson contends, his idea about pelagic larvae
and settling down on the sea bed at various stages works. This
implies protostomes versus deuterostomes is important (OVERHEAD)
The weak point, he admits is the derivation of deuterostomes
from the four holed trochaea, because there seems to be no very
good reason for it to happen that way.
Most respectable animals also have mesoderm. The derivation
of this third germ layer is also a problem. Mesoderm can arise
(OVERHEAD) from ectoderm (ectomesoderm) in the way we
are familiar with in the human head but this is an uncommon way
of making it. In flatworms, roundworms, molluscs annelids and
arthropods mesoderm comes from a small number of cells set aside,
rather like germ cells, early in development (4d mesoderm). In
echinoderms it arises as outpushings of the primitive gut in
the gastrula. There is nothing to suggest that 4d is ancestral
to endomesoderm or vice versa. It looks as if these two types
have evolved independently.
Coeloms also seem to have arisen separately in various groups. The logical classification would be acoelomates (coelenterates) versus coelomates (deuterostomes) but awkwardly protostomes seem to have a coelom too. If this is so then either:
the protostome coelom was derived from the deuterostome one
the deuterostome coelom was derived from the protostome one
the coelom evolved twice.
The answer is we don't know, but the first two don't work very well.
So we can set up at least two groups of animals, even if we
don't follow Nielsen all the way.
If these animals are all related to each other, as I suggest,
and the differences arose by changes in the development of different
kinds of animals then we have to start looking at how development
might be changed in some detail. What sorts of factors might
affect an egg as it develops? We can make a list: (OVERHEAD)
genome of offspring at fertilisation
Early views were that environmental agents affected developing
embryos directly - Lamarkism. The classic example of Lamarkism
relates to the tails of mice. Lamark said (in essence) if you
take a group of mice and cut off their tails, and continually
repeat this process, eventually mice will be born tail-less Evolutionary
change, recognised by small alterations of type, would thus produced
by environmental change, and the change is passed on to subsequent
Probably the first to test this was Geoffroy Saint-Hilaire.
Whilst Napoleon was in Egypt in 1799 Geoffroy made a grant application
for 600 chicken eggs, an incubator, 112 pairs of pigeons, ostrich
eggs, money for measuring instruments and salaries for assistants.
What was he doing? He was testing a theory that the sex of birds
was determined by egg shape. A little later we find him sealing
eggs with wax, removing them from the incubator for a day, soaking
them in water and sealing the oviducts of chickens to retain
eggs in 'a uterine environment'. What did he find?
Well the sex/egg shape ratio was wrong, but he did find changes,
such as retardations caused by cooling which he identified as
normal stages of lower vertebrates (recapitulation again). He
also found that growth in one element due to an increased blood
flow led to decrease in other elements. But on the whole he was
impressed by the limited amount of variation he could induce
in the common ground plan. The basics were not changed much by
the environment - and of course he had never heard of genetics.
So his theory was what we would now call epigenetic, that
development is modified by environment, and his conclusions largely
negative. The basic plan is conserved: awkward large changes,
such as the origin of birds by modification of limb structure
were christened saltatory - a great leap forward of unknown cause.
Constraints and the Bauplan.
The Bauplan seems then, fairly fixed, and we can only do so much to change it by modifying the environment. Why should this be? If evolution is random change then all aspects of development should be equally likely to vary. The fact that this is not so worried some people.(OVERHEAD) Whitman said ' but if organisation and the laws of development exclude some lines of variation and favour others there is certainly nothing supernatural in this and nothing which is incompatible with natural selection.'
Mayr suggested that 'some components of the phenotype are
built in far more tightly into the genotype than others' and
that 'certain components of the phenotype may remain unchanged
during phyletic divergence' 'Why is the chordate type so conservative
that the chorda is still formed in the embryology of tetrapods
and gill arches still in that of mammals and birds?'
These views imply that natural selection is not, in fact,
free to act randomly. Some structures are either protected from
change, or conservative or inert. In other words there are constraints
as to what may vary. Lets look at some of the possible constraints
that may exist.(OVERHEAD)
Structural constraints are more likely to affect unicellular
than multicellular organisms. Being very small may be a problem
because of external forces like Browning movement: being very
large may be a problem because of the need to transport things
from one side of the organism to the other by diffusion for instance.
Things like surface area/volume considerations have been eliminated
by forming colonies and eventually multicellular organisms. Other
mechanical constraints may affect the skeleton: you are not allowed
to construct a limb skeleton, say, that will not take the weight
of the organism it is supposed to support.
The maximum rate of mutation and the numbers of recombinations
formed will both constitute genetic constraints on evolutionary
change. We shall see later that some genes are phylogenetically
highly conserved, since we find them in many species and higher
taxonomic units. These are concerned with fundamental aspects
of development and so are somehow prevented from mutating or
have a very high priority service contract. We can imagine a
priority on any gene product, varying from absolute invariability
for the most vital, through partially restrained to free for
all. Free for all represents the maximum possible mutation rate:
anything less is constrained. Groups of characters may also be
associated genetically into suites, such as the suite of genes
that makes an upper limb : we recognise these by lack of genetic
covariance - i.e. they are all inherited together. The suite
of genes governing Aunt Maud's nose shape are less conserved.
Pleiotropy (the action of genes in multiple tissues) also acts
as a constraint. A particular gene may have two roles in two
different organs - it might make Darwin's tubercle on the ear
and that little wiggly bit on your little toe. If this is so
then you can't have one without the other. It has been argued
that the old 'one gene one enzyme' theory i.e. that one bit of
DNA makes one protein means that pleiotropism doesn't really
exist: this may be so but in practice during development genes
behave as if it does.
These are limits to variation brought about by the interdependence
of developmental processes, and constitute much of the content
of the rest of the course. They are recognised by the invariant
patterns which persist throughout morphology, and long periods
of evolutionary time. Maynard Smith defined them as 'biases on
the production of phenotypic variability brought about by the
nature of developmental systems'.
Limits to rates of cell division, secretion of cell products,
cell migration and/or metabolic efficiency are four examples
of cellular constraints. They are, of course, associated with
developmental constraints, because cells are what is developing.
A tissue which is dependent for its function on a good blood supply, in order to support a high metabolic rate, is limited in its capacity for change. A tissue with a low metabolic rate and no need for a good blood supply has more options. This is probably why cartilage is the most common supporting skeletal tissue in vertebrates and invertebrates, and appears often in ectopic tissue. Vascular tissue, like bone, is limited in its options.
A special case of metabolic constraint, especially in birds
and mammals is maternal metabolic constraint: if mum can't cope
then the offspring dies.
As embryos develop, and especially as functions like feeding
and respiration begin organ systems become functionally connected.
The skeleton of the jaws and branchial apparatus becomes involved
with the muscular system: the muscular system becomes involved
with the nervous system. The more of these links that develop
and the earlier they do so the more difficult it is to uncouple
one system in order to modify it. Think of the interrelations
of the mesonephros, the metanephros and the male and female reproductive
systems and ducts - very constrained by function.
Constraints and the Bauplan
The constraints that we have identified, and no doubt others,
have a huge effect on the Bauplan. Basically, they conserve it.
Individuals that conform to the Bauplan during development survive:
those that do not are eliminated. Spontaneous abortion, failure
to implant, embryonic and larval mortality are what ensure that
a frog's egg always gives rise to a frog and women have reasonably
Do we believe in the possibility of constraints and the elimination
of variation? Well, there is one good biological example of constraint
and perfect conservation - the genetic code. That varies very
little and presumably has huge constraints mechanisms built in
to preserve it.
So we can now make a statement: (OVERHEAD)
Variation associated with the production of the Bauplan
is minimal: constraints play a major role, and selection plays
a minor role. The role of selection is in fact negative:
those individuals that do not conform are selected against.
We may ask ourselves whether this statement is not the product of a circular argument? Those features that we have selected to be parts of the Bauplan are highly conserved, so of course they are not changed. This is the same circular argument that led Darwin to the selection of the fittest: who else but the fittest will survive? But if we don't take it too literally, and suggest that all constraints are 100% it is a decent working hypothesis: remember that some characters are more constrained than others.
Constraint outwith the Bauplan.
At a second level we have the other characteristics, those
which we have said are not part of the Bauplan. We must allow
these more freedom by definition (they are not constrained) and
allow mutation and selection to work on them. Constraint plays
a lesser role here.
One drawback is that this division immediately splits characters
into two leagues and necessitates first of all some sort of judgement,
presumably applied externally by us, as to whether something
is Bauplan or is not and secondly we need a mechanism to apply
constraints. Perhaps a more comfortable view is that constraint
can vary from 0-100%, and that we admit a character to the Bauplan
at, say, 60% constraint. - a purely nominal level. Below this
things are fairly easy to change, above this things are more
difficult. The more fundamental a thing is, or the more necessary,
then the bigger the lock on its chastity belt.
We now think we can begin to answer one question, why does
a frog's egg always produce a frog?- because of constraint The
next question is even tougher: how does an apparently simple
structure like an egg give rise to a complicated structure like
Well, it has to be preformation or epigenesis; either all
those structures are there already, and unfold like the homunculus,
or they gradually and progressively appear. If you are a preformationist
form already exists in the egg. If you are an epigenisist the
information necessary to define form exists in the egg. So epigenesis
(OVERHEAD) The sum of the genetic and non genetic
factors acting upon cells to selectively control the gene expression
that produces increasing phenotypic complexity during development.
The first to make a sensible comment on epigenesis was Aristotle,
who observed developing chick eggs and saw he progressive appearance
of new features, and how they were similar to developing fish
and mammals. He therefore came down as an epigenisist. The next
man to take this approach, and to improve on Aristotle was Coiter,
a Dutchman, 1800 years later.
But Aristotle was in a minority and between Aristotle and
Coiter most scientists were preformationists until Harvey and
Wolff persuaded the majority otherwise. Wolff saw clearly that
parts of the embryo developed from non-equivalent structures:
that blood vessels appeared where none were seen before and that
the tubular gut developed from a flat plate. Pander's discovery
of the germ layers in 1817 provided substance for Wolff's views:
structures arose from germ layers. Wolff also recognised, importantly,
that the sequence of appearances of parts both depended on pre-existing
parts and governed what was to come.
Teratological experiments such as those of Geoffery on eggs
proved that the malformed embryos were not preformed: he chose
eggs at random and applied treatment which caused the abnormalities.
If malformed embryos were not preformed then presumably neither
were his control normals.
The big problem however was this: preformationists believed
that the pre-existing structure was unfolded: very rational and
satisfying, even if there was a minor hiccough in the storage
of many generations, like Russian dolls, inside one another.
Epigenesis had the major snag of structures arising from non
existing structures - a good theory, but one as yet without a
mechanism behind it.
In the end it was probably regeneration that clinched the
issue for epigenesis. If you cut off an amphibian's limb, or
a tadpole's tail, or a Hydra's body it regrows. There is no sense
in which the regenerated part was present preformed in the amputation
stump. So in one way epigenisis is clearly the winner: embryonic
structures are not preformed in the egg. Yet in a sense we now
know preformation wins as well - because the instructions for
making a frog, rather than the frog itself, lie in the DNA of
the frog's egg.
But as well as the DNA the frog's egg contains other things:
organelles and cytoplasm. Are they implicated in development?
Yes of course they are, because in most organisms development
can proceed, at least for a time, without the zygotic nucleus.
This varies from the 2-4 cell stage in the mouse, through 4-8
cells in the pig, 8-16 cells in the sheep, to twelve divisions
(3-4000 cells) in Xenopus. This however, is a diversion:
development never goes the whole way without a nucleus.
How does development work then? We know that zygotes contain
copies of all the genes in the genome, and pass these on to their
descendants. We also know that not all genes are active in all
Lets now look at genetic and non genetic factors. Although they are likely to be complex and varied, and although we can't quite specify what they are at this stage, if there is any truth in epigenesis we should be able to see development as a hierarchical decision making process. Throughout there should be a series of decisions made by individual cells or groups of cells which are of this form: (OVERHEAD)
Do A/Don't do A
Do A/Do B.
Hierarchical systems have some interesting properties: some of these are common to hierarchies, and not a function of their content and they can evolve faster than non-hierarchical systems of similar size.
This page is maintained by Steve Paxton