Biology and Philosophy (2006) 21:553–558 DOI 10.1007/s10539-005-9001-y
Ó Springer 2006
The Nest’s Tale. A reply to Richard Dawkins PATRICK BATESON Sub-Department of Animal Behaviour, University of Cambridge, High street, Madingley, Cambridge, CB3 8AA, UK (e-mail:
[email protected]; phone: +47-55236370; fax: +47-55236379)
Key words: Causality, Evolution, Ontogeny, Teleology Abstract. If temperature does not vary from one generation from to the next but its value is crucial for the development of particular phenotypic characteristics, a long-term change in its value may trigger major evolutionary changes of the organism. If a bird’s nest maintains the critical temperature, then a statement that the bird is the nest’s way of making another nest is as helpful as accounts couched in terms of genes’ intentions. However, the language of intentions rests on different evidence and assumptions from causal language and the languages are not interchangeable. Understanding ontogeny in causal terms requires explanations that are made as simple as possible but not so simple that they become completely unrealistic.
The Extended Phenotype was Richard Dawkins’ most original book and deserved the attention it received in Biology and Philosophy. The three commentators, Kevin Laland, Scott Turner and Eva Jablonka stimulated a splendid and characteristic response from Dawkins (2004). However, a reference to an old joke of mine about the bird being the nest’s way of making another nest elicited this irritated denunciation: ‘Sterelny et al. (1996) go so far as to say ‘‘Bateson was right’’! No Bateson was not right, he wasn’t even close to being right’ (Dawkins 2004). He goes on: ‘... Bateson’s nest joke and others of this kind are not funny. There may be backwards arrows in all sorts of other senses but, in the sense that specifically matters for Darwinian evolution, the causal arrow of biological development from genotype to phenotype really is a one-way arrow’. I have little problem with this statement, although evidence that weakens its generality has started to accumulate (e.g. Jablonka and Lamb 2005). Dawkins (2004) referred to my ‘... superficially amusing but deeply misleading suggestion that a gene is a nest’s way of making another nest’. I first used the nest joke in my review of The Selfish Gene (Bateson 1978). It is worth quoting the passage in my review since the fidelity of the replication has suffered from Chinese Whispers, about which Dawkins writes so well, and, more seriously my intent had been corrupted over time. So much so, indeed, that I too had temporarily forgotten the point that I had wanted to make. What I actually wrote was this:
554 A legitimate focus on gene’s intentions should not be used as an excuse for resuscitating moribund preformationism. ... Dawkins accepts all this but then reveals his uncertainty about which language he is using by immediately giving special status back to the gene as the programmer. Consider a case in which the ambient environmental temperature during development is crucial for the expression of a particular phenotype. If the temperature changes by a few degrees the survival machine is beaten by another one. Would not that give as much status to a necessary temperature value as to a necessary gene? The temperature value is also required for the expression of a particular phenotype. It is also stable (within limits) from one generation to the next. It may even be transmitted from one generation to the next if the survival machine makes a nest for its offspring. Indeed, using Dawkins’ own style of teleological argument one could claim that the bird is the nest’s way of making another nest. Dawkins’ riposte to my tease was that nest material doesn’t have the permanence of DNA (Dawkins 1978). Later he developed the point, arguing that nests do not have the causal significance of genes. ‘There is a causal arrow going from gene to bird, but none in the reverse direction. A changed gene may perpetuate itself better than its unmutated allele. A changed nest will do no such thing unless, of course, the change is due to a changed gene, in which case it is the gene that is perpetuated, not the nest’. (Dawkins 1982, p. 98). Dawkins realised, however, that we might have been at cross purposes and on the next page wrote: ‘As is so often the case, an apparent disagreement turns out to be due to mutual misunderstanding. I thought Bateson was denying proper respect to the Immortal Replicator. Bateson thought that I was denying proper respect to the Great Nexus of complex causal factors interacting in development’. Dawkins 1982, p. 99). His ironic reference to the Great Nexus (not a phrase I have ever used) was not intended to be complimentary. Letting that pass for the moment, a deeper issue is at stake, namely the confusion that arises when a switch is made between different forms of thought. I was concerned that the undoubted power of the selfish gene language was being used to prop up the idea of the gene as ‘programmer’, but admittedly I distracted attention from this point by my joking suggestion that the teleological language could be played in different ways. I was not claiming that all the necessary conditions for development could be treated as ‘replicators’ in biological evolution. Nor was I making the vacuous statement that development is complicated. The central point of that passage in my review of The Selfish Gene was to do with the kind of conceptual slippage that can occur when language is used loosely. I suspect, that Dawkins believes that he has never been guilty of such slippage for he used the simile of the Necker Cube to refer to the ways it might be possible to move from one type of discourse to another. However, even as clear a thinker as Dawkins sometimes marches into a linguistic quagmire that causes a great deal of confusion.
555 Dawkins is aware that he uses ‘gene’ in distinctly different ways. For population geneticists, a genetic difference is identified by means of a biochemical, physiological, structural or behavioural difference between organisms (after other potential sources of difference have been excluded by appropriate procedures). Dawkins suggested that his move backwards and forwards between the language of gene intentions and the more orthodox language of genetic differences was acceptable because they are simply alternative ways of describing the same thing. To make his point, he described perception of the Necker cube. The front edges of the line drawing of the cube suddenly flip to the back as we look at them. The lines representing the edges of a cube can be seen as though either the top corner of the cube is facing forwards or it is facing away. Each perceived image of the cube is as real as the other and Dawkins suggests that, in similar ways, the different pictures of the gene translate backwards and forwards into the other (Dawkins 1982). Both perceptions are equally valid. At first the Necker Cube analogy seems appealing, but it is not exact because the bodies of thought and evidence on which perceptions are based are different for the two ways in which Dawkins uses ‘gene’. In the technically precise language of population geneticists, a genetic allele must be compared with another from which it differs in its consequences. In selfish-gene language, it stands alone as an entity, absolute in its own right. The perception generated by one meaning of gene does not relate to the same evidence as that generated by the other. Both Dawkins and I may be selfish, but the difference between us certainly is not. It makes no teleological sense to attribute motives to a comparison. The same issue arises in a different form in genetics when the switch is made from relative to absolute descriptions. Consider the problem when, in the course of evolution, an allele, defined in terms of a population difference, goes to fixation and all members of the population have a double complement of the allele. The other alleles, with which it was being compared, have ceased to exist and so has the relative basis for defining this gene. Of course, the DNA that made the crucial difference survives, but quite different scientific operations are required to demonstrate its existence. The message is that, we need to be very clear about the difficulties of translating from one language in to the other and the attendant confusions that arise when translation is careless or facile. While my nest talk should not be used in the context of Darwinian evolution, it might nevertheless throw up interesting questions about biological evolution in general that are not otherwise asked. It was this more general sense that may have led Sterelny et al. (1996) to claim that I was right about nests. Some aspects of the environment may be stable for a very long time and yet are crucial for the expression of an adaptive phenotype. Changes in those environmental factors can produce dramatic alterations in the phenotype. This thought lay behind Waddington’s (1957) interpretation of his own experiments when he changed environmental conditions and produced new phenotypes;
556 and it was central to his ideas about ‘genetic assimilation’. If previous environmental constants, such as the acidity of the sea, start to change, they can be major sources of extinction and more importantly they can provide the variation in phenotypes on which subsequent Darwinian evolution can act. This source of evolutionary change must not be confused with the adaptation that follows it, but it would be foolish to dismiss it as unimportant. That stated, I applaud Dawkins’ clear description of what usually matters in Darwinian evolution. Variants must breed true and with sufficient fidelity so that when one variant survives better or reproduces better than its alternative its characteristics are represented in subsequent generations. It is, as Dawkins would be the first to admit, a reformulation of Darwin’s mechanism for adaptive evolutionary change: variation, differential survival and onward transmission. The crucial agents necessary for this evolutionary process of adaptation will generally be genes. Nevertheless, Dawkins states that we should accept with open arms other agents or processes that might operate in the same way. Recently Mameli (2004) has responded to the challenge and extends the evolutionary mechanism in a disciplined way. Mameli asks us to consider the butterfly that lays its eggs on a particular plant the leaves of which are then eaten by its offspring caterpillars. The individuals retain through pupation some representation of what they have eaten and when the new generation of adult females butterflies have mated, they lay eggs on the particular species of plant they had eaten before metamorphosis. Occasionally the females lay their eggs on other species of plant. If the leaves should be more nutritious than those of the plants species usually eaten by the insects before metamorphosis, the caterpillars will grow faster and may survive better than their competitors. Consequently, without genetic change the butterfly species switches its plant of choice in the course of Darwinian evolution. In this case the variation lies in the behaviour of the adult female butterflies choosing sites for laying their eggs, the differential survival results from differences in nourishment and onward transmission to the next generation is achieved by an imprinting-like mechanism. Dawkins will probably argue that this and other instances like it are special cases and that they don’t seriously detract from the argument that, on the whole, the crucial variation on which the Darwinian evolution depends lies in genetic differences. I would agree with him. Nevertheless note that Mameli’s logic is tight and, interestingly, neither the replicator language nor the teleological account of the evolutionary process work very convincingly in the case he has given. It reminds us of the three types of question raised by the Darwinian evolutionary mechanism. What are the developmental and other processes that generate variation in the characteristics of organisms? What are the agents of differential survival and differential reproductive success? What are the necessary conditions for re-creating successful characteristics in the next generation?
557 Richard Dawkins (2004) had another go at me when he discussed the abuse of the term epigenetics which, he claimed, ‘... has become associated with obscurantism among biologists’. This is followed by a reference to a footnote which reads ‘I am reminded of a satirical version of Occam’s Razor, which my group of Oxford graduates mischievously attributed to a rival establishment: ‘‘Never be satisfied with a simple explanation if a more complex one is available’’. And that reminds me to say that Laland has missed the irony in my apparent espousal of Bateson’s ‘‘Great Nexus of complex causal factors interacting in development’’’. The mischievous attribution directed at me actually came from me. About 30 years ago I used to enjoy propounding what I called my three heterodox principles for people working on behaviour. The first was ‘Treat animals like humans until you have good reason to think otherwise’; the second ‘Never use a simple explanation if a more complicated one will do instead’; and the third ‘Never use a causal explanation if a teleological one will do instead’. The second one became known self-mockingly as the Cambridge principle because Robert Hinde, the driving intellect at the Sub-Department of Animal Behaviour at Cambridge, used to say repeatedly ‘Behaviour is complicated’. The third principle became known as ‘The Oxford Principle’ for reasons not unconnected with Richard Dawkins himself. The jokes were half serious, but only half. On the Cambridge principle, everyone will agree that an explanation of an organism’s development in terms of it merely getting larger is absurd. The thought that a homunculus inside the sperm head grew and grew until magically it became an airline pilot is not only simple, it is blatantly wrong. The opposite conclusion that everything is connected to everything else – the Great Nexus – is hopelessly vacuous and is not one I have ever derived or supported. My general concern has been with how the undoubted complexities of development might be made more tractable by uncovering principles that make sense of that complexity (e.g. Bateson 1976, 1991). As I see it, the impulse behind Robert Hinde’s easily lampooned phrase ‘Behaviour is complicated’ was a wish to provide an approach that is a precondition for constructing a sensible theory or for deriving a coherent principle. Many powerful voices had urged the behavioural and social sciences to model themselves on the success stories of classical physics or molecular biology. The obvious attractions of producing simple, easily understood explanations has meant unfortunately that crucial distinctions have been fudged in the name of being straightforward and analysis has been focussed on single factors in the name of clarity –as has been particularly obvious in studies of behavioural and cognitive development. Little progress is made in the end if the straightforwardness and clarity are illusions. Nobody likes to think that his or her pet principles are constrained. Indeed, a common feature of bolder writers is to make a virtue of this dislike and drive grossly stripped down explanations all over the place as though these were the attractive and necessary simplifications for which everybody craves.
558 Being complicated for its own sake has no merit either, but explanations are worthless if they do not bear some relation to real phenomena. Robert Hinde’s point was that understanding how the parts relate to each other is a precondition to understanding process and understanding process is the precursor to uncovering principles. Inevitably, tension still exists between those who emphasize differences and focus on complexity and those who attempt to unify and simplify. But given that there is no royal road, the old 1960s slogan ‘Make love, not war’ is worth remembering.
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