Griffiths 2.4.07

In P. Carruthers, S. Laurence & S. Stich (Eds.), The Innate Mind: Culture and Cognition.
Oxford: Oxford University Press, 2006: 91-101.

6 The Baldwin effect and genetic assimilation: contrasting
explanatory foci and gene concepts in two approaches to an
evolutionary process
Paul E. Griffiths
1 The Papineau Effect

David Papineau (2003; 2005) has discussed the relationship between social learning and the
family of postulated evolutionary processes that includes organic selection, coincident
selection, autonomisation, the Baldwin effect and genetic assimilation. In all these
processes a trait which initially develops in the members of a population as a result of some
interaction with the environment comes to develop without that interaction in their descendants.
It is uncontroversial that the development of an identical phenotypic trait might depend on an
interaction with the environment in one population and not in another. For example, some
species of passerine songbirds require exposure to species-typical songs in order to reproduce
those songs whilst others do not. Hence we can envisage a species beginning with one type of
developmental pathway and evolving the other type. If, however, the successive evolution of
these two developmental pathways were a mere coincidence, selection first favoring the ability to
acquire the trait and later, quite independently, favoring the ability to develop it autonomously,
then this would not be a distinctive kind of evolutionary process, but merely two standard
instances of natural selection. George Gaylord Simpson pointed this out in the paper that gave us
the term Baldwin effect (Simpson, 1953). The real interest of the Baldwin effect and its
relatives lies in the mechanisms which might link the evolution of the two developmental
pathways, so that acquiring the trait through interaction with the environment makes it more
likely that later generations will evolve the ability to acquire the same trait without that
interaction.
Papineau focuses on the way in which social learning can facilitate such Baldwin-like
links. His basic idea is that the genes which accelerate the social learning of some complex
behaviour might become advantageous only if that behaviour is already being passed on by
learning in an animal culture. In this scenario the relevant genes would be selected once the
1
population is socially transmitting the behaviour, but not otherwise, thus yielding a scenario that
satisfies the specifications of the Baldwin effect. Papineau subjects this sort of process to closer
analysis, showing that it simultaneously exemplifies two different kinds of mechanism that the
literature recognizes as possible sources of Baldwin effects. First, there is the process that
Papineau calls genetic assimilation. Here the focus is on some complex adaptive behaviour,
potentially under the control of a suite of genes at different loci. The challenge is to explain how
this suite can get selected in virtue of their collectively producing the complex adaptive behavior.
Prima facie, it seems that the whole suite of genetic changes would need to occur simultaneously.
An answer becomes available if the complex behaviour is also learnable, for then each gene can
be advantageous on its own, in virtue of making the rest of the behaviour more quickly or more
reliably learnable. The cumulative selection of the whole suite of genes thus qualifies as a
Baldwin effect because it depends essentially on intermediate stages in which (most of) the
behaviour is learned.
This is one part of what Papineau thinks occurs in social learning cases. But he observes
that there is a yet further sense in which such cases fit the Baldwin requirements. The process he
calls genetic assimilation takes it as given that the complex behaviour at issue is indeed
learnable. But in many cases it will be puzzling in itself that some complex behaviour can be
learned, at least insofar as instrumental learning is supposed do the work, and reward only
accrues once the whole behaviour is in place. This is where social learning plays its role: if the
behaviour is present in the animal culture, then this in itself can render it learnable and so
genetically assimilable. This now gives us a second sense in which Papineaus social learning
cases are Baldwin effects: the behaviour is only individually-learnable-and-so-genetically-
assimilable because it is already present as a learned behaviour in the animal culture.
Papineau suggests that this sort of double-strength Baldwin effect will exert powerful
selection pressures in species that exhibit a high degree of social learning. This is an interesting
empirical conjecture that may or may not prove correct. For my part, I am happy to agree that
social learning can play a role in a distinctive form of niche-construction (Odling-Smee et al.,
2003) that can alter selective pressures in the way Papineau suggests.
I shall say nothing more here about social learning. Rather I want to focus on Papineaus
discussion of genetic assimilation. This term was introduced by Conrad H. Waddington to refer
to a specific process (Waddington, 1942, 1953). Waddingtons process stands out among the
other ideas listed above (organic selection, coincident selection, autonomisation, the
2
Baldwin effect) both because Waddington was able to demonstrate it in laboratory selection
experiments and because it was part of his larger vision of the relationship between development
and evolution, a vision that has influenced contemporary work in evolutionary developmental
biology or evo-devo.
Let us look more closely at the way Papineau defines Waddingtons Genetic
Assimilation. He says:
Suppose 5 sub-traits, say, are individually necessary and jointly sufficient for T.
Each can either be genetically fixed or acquired through (not necessarily social)
learning. (So for sub-trait TK we have allele KG which genetically fixes TK and
allele KL which allows it to be learned.)
Suppose also that at first the KGs are rare. Still, those lucky organisms that
have some TKs genetically fixed by KGs will find it easier to learn the rest of T,
and so will be favoured by natural selection (assuming that learning is here
costly). Selection will thus cumulatively build up the genes KG which genetically
fix T.
(Papineau, 2003)
This process has little connection with the one described by Waddington himself 1. In
itself this is neither particularly important nor particularly surprising. Many different processes
have been proposed that might free traits from their developmental dependence on some aspect
of the environment, and terms like Baldwin effect and genetic assimilation have been used in
numerous senses in this extensive literature (See e.g. Belew and Mitchell, 1996; Weber and
Depew, 2003). In fact, despite calling the process Waddingtons genetic assimilation Papineau
does not cite Waddingtons work as a source, but instead cites a well-known computer simulation
of the interaction between learning and inheritance (Hinton and Nowlan, 1996). The interesting
point is that Waddingtons actual model of genetic assimilation is simply not accessible to
anyone who conceptualises genes in the way Papineau does in the passage quoted above. Several
1
It does resemble one version of organic selection. Patrick Bateson has argued that many learning processes have
components which might separately become independent of the environmental conditions originally required for
their development and that the efficiency and/or reliability of the learning process might thereby be improved.
Like Papineau, he points out that these variations would only be selected if organisms regularly undergo the
complete learning process (Bateson 2004, 289).
3
recent authors have stressed the need for biologists and philosophers of biology to become more
self-conscious about the existence of multiple gene concepts and of the appropriate range of
theoretical and experimental contexts in which those concepts should be deployed (Moss, 2002;
Falk, 2000; Stotz et al., 2004; Griffiths and Neumann-Held, 1999). I will argue here that paying
attention to gene concepts helps one to distinguish two radically different approaches to
explaining how the development of a phenotypic trait can become independent of certain aspects
of the developmental environment. One approach looks to selection to forge a link between the
successive evolution of two developmental pathways to the same trait. The other approach,
represented by Waddingtons genetic assimilation, looks to developmental biology. This latter
approach seeks to explain how the development of a phenotypic trait can become independent of
an environmental stimulus (or become dependent on that stimulus) by showing that in certain
kinds of developmental systems such transitions can be produced by small genetic changes
changes that are likely to occur spontaneously in a relatively short time. In the first approach the
explanatory focus is on the relative selective advantage of the two developmental pathways. In
the second approach the explanatory focus is on the developmental mechanisms that make
suitable variants available for selection.
2 Genetic assimilation and Gene-P

In the passage quoted above Papineau employs a concept of the gene which Lenny Moss has
labeled Gene-P:
Gene-P is defined by its relationship to a phenotype. Gene-P is the expression

of a kind of instrumental preformationism (thus the P). When one speaks of a
gene in the sense of Gene-P one simply speaks as if it causes the phenotype. A
gene for blue eyes is a Gene-P. What makes it count as a gene for blue eyes is not
any definite molecular sequence (after all, it is the absence of a sequence based
resource that matters here) nor any knowledge of the developmental pathway that
leads to blue eyes (to which the "gene for blue eyes" makes a negligible
contribution at most), but only the ability to track the transmission of this gene as
a predictor of blue eyes. Thus far Gene-P sounds purely classical, that is,
Mendelian as opposed to molecular. But a molecular entity can be treated as a
Gene-P as well. BRCA1, the gene for breast cancer, is a Gene-P, as is the gene for
4
cystic fibrosis, even though in both cases phenotypic probabilities based upon
pedigrees have become supplanted by probabilities based upon molecular probes.
(Moss, 2001, p. 87-88)
Papineaus five genes are Gene-Ps, each defined by a specific part (sub-trait) of the
phenotypic trait T. I take it that these parts are dispositions to acquire behavioral modifications
which together amount to a disposition to acquire the new behavior T. The process he labels
genetic assimilation is therefore simply the spread of certain of these phenotypic traits as a
result of selection. His trait KG is selectively superior to KL because KG individuals acquire T
more reliably than KL individuals. The sought-for link between individuals initially learning the
sub-trait K and later individuals possessing K without learning is mediated by a process of niche
construction a change in the selective regime as a result of behavior. In contrast, Waddington
thought that the link between the ability to reliably acquire an adaptive trait and the appearance
of individuals with an intrinsic tendency to exhibit that trait was forged by the typical nature of
the development pathways underlying adaptively valuable traits. It was for this reason that he
objected to Simpsons term Baldwin effect with its implication that this evolutionary process is
a special case. Waddington intended genetic assimilation to be a ubiquitous feature of phenotypic
evolution:
Simpson comes to the conclusion that the Baldwin effect, in the sense he
describes it, has probably played a rather small role in evolution. The genetic
assimilation mechanism, however, must be a factor in all natural selection, since
the properties with which that process is concerned are always phenotypic;
properties, that is, which are the products of genotypes interacting with
environments.
(Waddington, 1953, p. 386)
According to Waddington the tendency of phenotypes to become genetically assimilated

reflects the fact that there is little difference between the actual developmental processes that
underlie a highly canalised phenotype that depends on an environmental stimulus and one that
has been rendered independent of that stimulus, as I will now try to explain.
5
3 Genetic assimilation and Gene-D
Waddington was aware that his vision of development required a conception of the gene which
does not intrinsically link genes and specific phenotypic outcome. He made this point in The
Evolution of Developmental Systems, an address delivered in Brisbane in 1951:
Some centuries ago, biologists held what are called preformationist theories of
development. They believed that all the characters of the adult were present in the
newly fertilized egg, but packed into such a small space that they could not be
distinguished with the instruments then available. If we merely consider each
gene as a determinant for some definite character in the adult (as when we speak
loosely of the gene for blue eyes, or for fair hair), then the modern theory may
appear to be merely a new-fangled version of the old idea. But in the meantime,
the embryologists, who are concerned with the direct study of development, have
reached a quite different picture of it This is the theory known as epigenesis,
which claims that the characters of the adult do not exist already in the newly
fertilized germ, but on the contrary arise gradually through a series of causal
interactions between the comparatively simple elements of which the egg is
initially composed. There can be no doubt nowadays that this epigenetic point of
view is correct.
In Waddingtons vision of development, the entire collection of genes makes up a

developmental system which produces a phenotype. Many features of the phenotype are
explained by the dynamical properties of that developmental system as a whole, rather than by
the influence of one or a few specific alleles. Thus, for example, Waddington sought to explain
one of the major biological discoveries of his daythe fact that extreme phenotypic uniformity
can be observed in many wild populations despite extensive genetic variation in those same
populationsby appealing to the global dynamics of developmental systems. A canalised
developmental system takes development to the same endpoint from many different genetic
starting points. The development of wild-type phenotypes can thus be buffered against genetic
variation. Waddington represented this idea with his famous developmental landscape (Figure
1).
6
Figure 1. Waddington's developmental landscape. (a) The developmental trajectory of

the organism, represented by the rolling ball, is determined by a landscape representing the
developmental dynamics of the organism. (b) The shape of this landscape is determined by
genes, here represented by pegs pulling the landscape into shape via strings, and by epistatic
interactions between genes, here represented by connections between strings. From Waddington
(1957: 36).2
2
Note to editor: Copyright request to: Allen & Unwin Ltd., 19 Crompton Terrace, London, N1
2UN, for pg.36 of 'The Strategy of the Genes - A Discussion of Some Aspects of Theoretical
Biology'; C.H. Waddington; Ruskin House (copyright George Allen & Unwin Ltd.); 1957.
7
In modern terms, Waddingtons developmental landscape is a representation of
development as complex system whose parameters are genetic loci and whose state space is a set
of phenotypic states. The state space is depicted as a surface, each point of which represents a
phenotype. The genetic parameters are depicted as pegs that pull on the surface and thus
determine its contours. Epistatic interactions between loci are represented by links between the
cords by which those loci pull on the surface. The development of an organism over time is
represented by the movement of a ball over the surface, which is dictated by gravity, so that the
ball rolls downhill on a path dictated by the contours of the surface. The development of the
organism is thus represented by its trajectory over the surface, through successive phenotypic
states. The basic point which Waddington uses this representation to make is that if the surface
has any significant contours, then the effect of a change at one genetic locus will be dictated by
the overall shape of the landscape, which is a global consequence of the states of all the other
genetic loci. Some genetic changes, such as those which affect the tops of inaccessible hills,
will have no effect on development. Other changes of the same intrinsic genomic magnitude
which affect the entrance of a valley or canal will have a massive effect on development. The
phenotypic impact of a genetic change is not proportional to the magnitude of the genomic
change, but depends on the overall dynamics of development. Furthermore, the phenotypic
difference produced by a genetic difference is not explained by that genetic difference in itself,
but by how that change interacts with the rest of the developmental system. This picture retains
considerably validity in the light of contemporary developmental genetics (Gilbert, Opitz, and
Raff, 1996; Wilkin, 2003)
Thus, in Waddingtons vision, phenotypes are global expressions of genomes, but it does
not follow that particular parts of the phenotype express particular parts of that genome. The
gene concept that fits this thoroughly epigenetic view of development is the one which Moss has
labeled Gene-D:
Quite unlike Gene-P, Gene-D is defined by its molecular sequence. A Gene-D is a

developmental resource (hence the D) which in itself is indeterminate with
respect to phenotype. To be a gene for N-CAM, the so-called neural cell
adhesion molecule, for example, is to contain the specific nucleic acid sequences
from which any of a hundred potentially different isoforms of the N-CAM protein
may potentially be derived N-CAM molecules are (despite the name) expressed
8
in many tissues , at different developmental stages, and in many different forms.
The phenotypes of which N-CAM molecules are co-constitutive are thus highly
variable, contingent upon the larger context, and not germane to the status of N-
CAM as a Gene-D.
(Moss, 2001, p. 88, emphases in original)3
To understand Waddingtons vision of development it is essential not to think of genes as

genes for particular phenotypes or phenotypic differences (Gene-P), but instead to think of
them as parameters of a developmental system (Gene-D). It is necessary to think in terms of
what in Waddingtons day was known as physiological genetics.
In a series of widely-read papers the philosopher Andre Ariew has used Waddingtons
concept of canalisation to explicate the concept of innateness (Ariew, 1996, 1999). Innate traits,
Ariew has argued, are those traits insensitive to environmental variation, or, equivalently, those
traits which are canalised with respect to changes in the environmental parameters of a
developmental system. Unfortunately, Ariews work has led philosophers who know of
Waddington only through these papers to use the term canalisation and even genetic
canalisation to mean insensitivity to environmental variation. In fact, the idea of insensitivity to
environmental factors, properly known as environmental canalisation (Wagner, Booth, and
Homayoun, 1997), cannot even be represented in Waddington classic picture of the
developmental landscape (Figure 1). Environmental parameters are not included in this model,
and whether a phenotype is canalised in Waddingtons original sense is a question of the
dynamical structure of the developmental system, not the relative role of genes and
environment.4 But the model can easily be extended to include environmental parameters, and
Waddington himself does so when discussing genetic assimilation, as seen below. If these
additional parameters are added, then we can define both environmental canalisation and
genetic canalisation. A phenotypic outcome is environmentally canalised if those features of the
3
Philosophers will note that Gene-P and Gene-D correspond respectively to descriptive and rigid readings of the
phrase the gene for T when this phrase is used in the usual way to report the fact that some DNA sequence
accounts for a large portion of the variance in trait T in some study population (See Sterelny and Griffiths, 1999, p.
90-92).
4
The evolutionary developmental biologist Brian Hall has written extensively on Waddington and has stressed that
his thought was profoundly gene centered in the sense that he saw the developmental system as primarily and
predominantly the expression of a potential present in the genome (Hall, 2003, 1992, 1999).
9
surface which direct development to that endpoint are relatively insensitive to the manipulation
of environmental parameters. A phenotypic outcome is genetically canalised if those features of
the surface which direct development to that endpoint are relatively insensitive to the
manipulation of genetic parameters. It should be noted, however, that we are not forced to draw
this distinction. The idea of canalisation with respect to all the parameters that are included in a
model of the developmental system is equally legitimate. It is, after all, far from clear whether to
classify many critical parameters, such as the presence of DNA methylation or of maternal gene
products in the cytoplasm, as genetic or environmental. The issue of genes versus
environment is peripheral to Waddingtons central concern, which is how developmental
outcomes can be robust and reliable in the face of variations in developmental parameters.
Like some modern authors, Waddington believed that natural selection would favor the
canalisation of important adaptive phenotypes. Developmental systems that produce important
adaptive outcomes robustly will be selected over those that are easily perturbed. Although I do
not have time to explore this theme fully here, it is important to recall that, like his
contemporaries I.I Schmalhausen and Theodosius Dobzhansky, Waddington saw natural
selection as optimizing, not the phenotypic character itself, but rather a norm of reaction which
specifies a range of phenotypes as a function of genetic backgrounds and environmental
conditions: An animal is, in fact, a developmental system, and it is these systems, not the mere
static adult forms which we conventionally take as typical of the species, which become
modified in the course of evolution (Waddington, 1952, 155). When there is a single, optimal
phenotype, stabilising selection will operate to select a narrow reaction norm, or, in other
words, to canalize the phenotype. In other circumstances, however, selection may favour a
broader reaction norm, producing what we describe today as adaptive phenotypic plasticity.
The shape of the norm of reaction is itself a character produced by natural selection.
We are now in a position to see why Waddington thought there would be little difference
between the actual developmental processes that underlie a highly canalised phenotype that
depends on an environmental stimulus and those that underlie one that has been rendered
independent of that stimulus. Waddington writes:
If natural selection was in this way acting in favour of the ability to respond in a
useful way to some environmental stimulus, it would also in time build up a
canalised response, so that the most valuable degree of expression was regularly
10
achieved. Once that had been done, the genotype would have been modified so
that it determined a new valley on the developmental surface; but it would still
require the push of an environmental stimulus to cause one of the balls in our
model to run into it. However, once the valley was formed and canalised, the
exact strength of the push, and the exact time at which it was applied, would be of
lesser importance. In fact, we might expect that, by this stage in the evolution
[sic], there would be a number of mutant genes available in the species which
could divert development into the prepared channel; and thus, once the ground
had been prepared, as it were, an internal genetic mechanism could take over from
the original environmental stimulus. We can thus envisage a mechanism by which
a valuable response to the environment could become gradually incorporated into
the hereditary endowment of the species.
I have discussed elsewhere how some of Waddingtons contemporaries, particularly J.B.S

Haldane and his wife and collaborator Helen Spurway, saw his work on genetic assimilation as
demonstrating that there need be little difference as regards developmental genetics between
innate and acquired traits (Griffiths, 2004). Haldane and Spurway drew on Waddington to
argue that transitions back and forth between instinct and learning were to be expected in
response to the adaptive advantages of these two forms of development in specific environments.
A couple of brief quotations will give the flavour of this work:
[discussing passerine song learning] some of these species must have passed
through a stage where the song was learnt by some individuals and was instinctive
in others. As a geneticist I think that it is quite impossible to make a sharp
distinction between learnt and unlearnt behavior.
(Haldane, 1992 [1955], p. 605).
The number of generations during which a learned ethogenesis evolves into an

instinctive ethogenesis, if it does so at all, depends on the relative strength of the
selection pressures favouring uniformity and variability in development.
(Haldane and Spurway, 1954, p. 275)
11
One of the most exciting features of this, Waddingtonian, vision of transitions between
instinct and learning is its symmetry. Most accounts of the Baldwin effect and its relatives focus
exclusively on the elimination of dependence on an environmental factor, but the mechanisms
underlying Waddingtons genetic assimilation can equally lead to environmental assimilation
when the selection pressures are reversed. Baldwinian phenomena are thus subsumed under the
more general topic of the selective advantages of different patterns of interaction between gene
and environmentthe field of research known today as adaptive phenotypic plasticity
(Brakefield and Wijngaarden, 2003; Schlichting, 2003). The traditional emphasis on the Baldwin
effects and its relatives to the exclusion of other evolutionary patterns reflects a misguided desire
to get the effects of the environment on development written into the germline, which in turn
reflects the mistaken conviction that only in this way can the effects of the environment on
development be of evolutionary significance (Griffiths, 2003).
4 Gene concepts and explanatory foci

In the evolutionary scenario described by Papineau the gene for trait K (allele K G) spreads
through the population in response to a selection pressure caused by the spread of a learnt trait T
whose acquisition requires five separate dispositions each of which corresponds to a gene (allele
KL and four companions). As I remarked above, these genes are Gene-Ps they are DNA
elements individuated by the criteria that their presence is a reliable statistical predictor of a
phenotypic difference. This, I suggest, is typical of one way of thinking about how the
development of a phenotypic trait can become independent of certain aspects of the
developmental environment. The evolutionary problem is framed as follows: 1) What are the
adaptive advantages of having T conditional on an environmental factor? 2) What are the
adaptive advantages of having T independent of that factor? 3) Does the evolution of the first
trait produce new selection pressures which favour the evolution of the second? The genes that
feature in typical scenarios designed to address these questions are Gene-Ps corresponding to the
difference between the first trait and the second.
In contrast, most of the genes that figure in Waddingtons genetic assimilation scenario
the pegs in Figure 1 are genes that are present both when the trait is dependent on the
environment and when it is independent of the environment. They are the genes (Gene-Ds)
which play a causal role in building the K phenotype, not the genes that differ between cases
12
where that particular cascade of gene expression is switched on endogenously and cases where it
is switched on exogenously or even the genes that differ between individuals that have K and
those that lack K. The evolutionary problem is framed as follows: How does evolution produce
traits which can be readily switched between different triggers? This second way of thinking
about how the development of a phenotypic trait can become independent of certain aspects of
the developmental environment corresponds to some of major themes in recent evolutionary
developmental biology, namely the evolution of developmental modularity (Gass and Bolker,
2003; Wagner, 2001) and the evolution of phenotypic plasticity (Preston and Pigliucci, 2004;
Gilbert, 2001; Brakefield and Wijngaarden, 2003). These evolutionary problems simply cannot
be posed if evolution is represented as change over time in the frequency of genes for specific
phenotypes (Gene-Ps).
We can compare these two ways of thinking about how the development of a phenotypic
trait can become independent of certain aspects of the environment with two ways to approach
the evolution of sexual differentiation. The primate SRY gene on the Y chromosome is a Gene-P
with respect to the masculinisation of the foetus: individuals who have this gene are very likely
to have a male phenotype. But it does not follow that the evolution of sexual differentiation
should be studied by asking how the SRY gene evolved. The masculinisation of the mammalian
foetus is the result of a complex cascade of a gene expression. Both male and female foetuses
have almost all the genes involved in this cascade. In Waddingtons terms the developmental
landscape has a deep branching valley running across it and the SRY gene, or its equivalent in
other mammals, simply nudges the foetus into one branch rather than the other. With this picture
in mind, it is easy to understand how two rodents of the genus Ellobius have managed to lose the
whole Y chromosome whilst retaining the gene expression cascade of mammalian sexual
development. Some other gene expression event early in development acts to triggers the same
cascade. Furthermore, sexual differentiation is an ancient characteristic of vertebrates and in this
larger group cascades of gene expression that are to some degree homologous with those in
mammals are triggered in still more diverse ways. Crocodiles, amongst others, have
environmentally triggered sexual differentiation. Some fish retain the capacity for females to be
masculinised by an environmental trigger throughout their life cycle. From the viewpoint of
developmental genetics, understanding the evolution of the specific triggering cause in one group
or another is not the way to understand the evolution of the cascade of gene expression which
constitutes becoming male. Nevertheless, there is nothing wrong with Gene-P thinking in the
13
right contextif we want to ask about the evolutionary pressures leading to genetic versus
environmental sex determination it is appropriate to pose the question in terms of the selection
pressures on the specific loci involved in these two modes of triggering. In the same way, we can
examine the selection pressures on the specific loci involved in making the switch between the
dependence of a behavior on learning and its independence of learning, as Papineau does, but
this should not be confused with the quite different project in which Waddington was engaged,
namely asking how developmental systems make such options readily available to selection.
5 Conclusion
Many evolutionary processes have been described in which a trait that initially develops in the
members of a population as a result of some interaction with the environment comes to develop
without that interaction in their descendants. Waddingtons genetic assimilation is importantly
different from the rest of this Baldwiniana because his explanatory focus was not on the
selection pressures at the point of transition, but on how developmental systems come to be
structured in such a way that these evolutionary transitions are readily accessible to evolving
lineages. Waddingtons approach also replaces the simple contrast between acquired and
innate with a non-dichotomous model of developmental canalisation and phenotypic plasticity
that is in line with recent work on the evolution of development. From a Waddingtonian
perspective evolutionary transitions between innate and acquired are only to be expected
because those categories have little meaning in terms of developmental genetics and in some
cases the difference between the innate and acquired may require only a minimal change in
developmental mechanisms. But to see this it is necessary to use a gene concept suitable for
thinking about development, and not a gene concept designed for theoretical population genetics
or for the prediction of phenotypic differences within populations.
References
Ariew, A. 1996. Innateness and canalization. Philosophy of Science, 63 (3 (Supplement)).
Ariew, A. 1999. Innateness is canalization: In defense of a developmental account of innateness.
In V. G. Hardcastle (ed.), Where Biology Meets Psychology: Philosophical Essays. MIT
Press.
Bateson, P. 2004. The active role of behaviour in evolution. Biology & Philosophy, 19 (2).
14
Belew, R.K, and Mitchell, M. (eds.) 1996. Adaptive Individuals in Evolving Populations.
Addison-Wesley.
Brakefield, P. M. and Wijngaarden, P. J. 2003. Phenotypic plasticity. In B. K. Hall and W. M.
Olson (eds.), Keywords and Concepts in Evolutionary Developmental Biology. Harvard
University Press.
Falk, R. 2000. The Gene: A concept in tension. In P. Beurton, R. Falk and H. J. Rheinberger
(eds.), The Concept of the Gene in Development and Evolution. Cambridge University Press.
Gass, G. L. and Bolker. J. M. 2003. Modularity. In B. K. Hall and W. M. Olson (eds.), Keywords
and Concepts in Evolutionary Developmental Biology. Harvard University Press.
Gilbert, S. F., Opitz, J. M. and Raff, R. A. 1996. Resynthesising evolutionary and developmental
biology. Developmental Biology, 173.
Gilbert, S. F. 2001. Ecological developmental biology: Developmental biology meets the real
world. Developmental Biology, 233.
Griffiths, P. E. 2003. Beyond the Baldwin effect: James Mark Baldwin's 'social heredity',
epigenetic inheritance and niche-construction. In B. H. Weber and D. J. Depew (eds.)
Evolution and Learning: The Baldwin Effect Reconsidered. MIT Press.
Griffiths, P. E. 2004. Instinct in the '50s: The British reception of Konrad Lorenz's theory of
instinctive behaviour. Biology and Philosophy, 19 (4).
Griffiths, P. E. and Neumann-Held, E. M. 1999. The many faces of the gene. BioScience, 49 (8).
Haldane, J. B. S. 1992 [1955]. Animal communication and the origin of human language.
Current Science, 63 (9-10).
Haldane, J. B. S. and Spurway, H. 1954. A statistical analysis of communication in "Apis
Mellifera" and a comparison with communication in other animals. Insectes Sociaux 1 (3).
Hall, B. K. 1992. Waddington's legacy in development and evolution. American Zoologist, 32.
Hall, B. K. 1999. Evolutionary Developmental Biology. 2 ed. Kluwer.
Hall, B. K. 2003. Baldwin and beyond: Organic selection and genetic assimilation. In B. H.
Weber and D. J. Depew (eds.), Evolution and Learning: The Baldwin Effect Reconsidered.
MIT Press.
Hinton, G.E, and Nowlan, S. J. 1996. How learning can guide evolution. In R. K. Bewel and M.
Mitchell (eds.), Adaptive Individuals in Evolving Populations. Addison-Wesley. First
published in, Complex Systems 1, p. 495-502. Technical report CMU-CS-86--128, Carnegie
Mellon University. 1987.
15
Moss, L. 2001. Deconstructing the gene and reconstructing molecular develomental systems. In
S. Oyama, P. E. Griffiths and R. D. Gray (eds.), Cycles of Contingency: Developmental
Systems and Evolution. MIT Press.
Moss, L. 2002. What Genes Can't Do. MIT Press.
Odling-Smee, F. Laland, J. K. and Feldman, M. W. 2003. Niche Construction: The Neglected
Process in Evolution: Vol. 37, Monographs in Population Biology. Princeton University
Press.
Papineau, D. 2003. The Baldwin Effect and social learning. Paper read at Innateness and the
Structure of the Mind, July 2003, at Sheffield.
Papineau, D. 2005. Social learning and the Baldwin effect. In A. Zilho (ed.), Cognition,
Evolution, and Rationality. Routledge.
Preston, K, and Pigliucci, M. (eds.). 2004. The Evolutionary Biology of Complex Phenotypes.
Oxford University Press.
Schlichting, C. D. 2003. Environment. In B. K. Hall and W. M. Olson (eds.), Keywords and
Concepts in Evolutionary Developmental Biology. Harvard University Press.
Simpson, G. G. 1953. The Baldwin effect. Evolution, 7.
Sterelny, K. and P. E. Griffiths. 1999. Sex and Death: An Introduction to the Philosophy of
Biology. University of Chicago Press.
Stotz, K. and Griffiths, P. E. and Knight, R. D. 2004. How scientists conceptualise genes: An
empirical study. Studies in History & Philosophy of Biological and Biomedical Sciences
(December) 35 (4).
Waddington, C. H. 1942. Canalisation of development and the inheritance of acquired characters.
Nature, 150.
Waddington, C. H. 1952. The evolution of developmental systems. Paper read at Twenty-eighth
Meeting of the Australian and New Zealand Association for the Advancement of Science, at
Brisbane, Australia.
Waddington, C. H. 1953. The "Baldwin Effect", "Genetic Assimilation" and "Homeostasis".
Evolution, 7.
Waddington, C. H. 1953. Genetic assimilation of an acquired character. Evolution, 7.
Wagner, G. P. (ed.). 2001. The Character Concept in Evolutionary Biology. Academic Press.
Wagner, G. P. Booth, G. and Homayoun, B. C. 1997. A population genetic theory of canalization.
Evolution, 51.
16
Weber, B. H. and Depew, D. J. (eds.). 2003. Evolution and Learning: The Baldwin effect
Reconsidered. MIT Press.
Wilkin, A. 2003. Canalization and genetic assimilation. In B. K. Hall and W. M. Olson (eds.),
Keywords and Concepts in Evolutionary Developmental Biology. Harvard University Press.
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In P. Carruthers, S. Laurence & S. Stich (Eds.), The Innate Mind: Culture and Cognition.

Oxford: Oxford University Press, 2006: 91-101.

1 The Papineau Effect

2 Genetic assimilation and Gene-P

Gene-P is defined by its relationship to a phenotype. Gene-P is the expression

According to Waddington the tendency of phenotypes to become genetically assimilated

In Waddingtons vision of development, the entire collection of genes makes up a

Figure 1. Waddington's developmental landscape. (a) The developmental trajectory of

Quite unlike Gene-P, Gene-D is defined by its molecular sequence. A Gene-D is a

To understand Waddingtons vision of development it is essential not to think of genes as

I have discussed elsewhere how some of Waddingtons contemporaries, particularly J.B.S

The number of generations during which a learned ethogenesis evolves into an

4 Gene concepts and explanatory foci

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