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Biology and Philosophy 19: 377–396, 2004.
© 2004 Kluwer Academic Publishers. Printed in the Netherlands.
Extended Phenotype – But Not Too Extended. A Reply
to Laland, Turner and Jablonka
RICHARD DAWKINS
University Museum of Natural History, University of Oxford, UK
I am grateful to the three commentators for their thoughtful and penetrating
remarks, and to the Editor for commissioning them. All three have forced me
to think, re-opening neural pathways that had suffered neglect as I turned to
other things in the years since The Extended Phenotype (henceforth EP) was
published. Their essays raise so many interesting points, it would take another
book to reply to them properly. Instead, on the basis that it is better to say a
few things thoroughly than lots sketchily, I shall concentrate on what I take
to be each author’s central argument.
J. Scott Turner and Kevin Laland both, in their different ways, want to
go further than me in extending the phenotype. Or so they see it. I am not
so sure that further is the right word. Progress implies movement in a useful
direction, whereas their extensions – of the organism, and into niche creation
– occasionally reminded me of Stephen Leacock’s knight who jumped on
his horse and galloped off in all directions. I don’t intend that flippantly or
disrespectfully. The relevant point about the extended phenotype is that it is
a disciplined extension. There are lots of other tempting ‘extensions’, which
sound similar but take us off in misleading directions. I have always fought
shy of misapplying the phrase to a profligate range of apparently plausible
extensions.
To take a more extreme example than these commentators consider, when
I am asked by lay people (as I frequently am) whether buildings count as
extended phenotypes, I answer no, on the grounds that the success or failure
of buildings does not affect the frequency of architects’ genes in the gene
pool. Extended phenotypes are worthy of the name only if they are candidate
adaptations for the benefit of alleles responsible for variations in them. I might
admit the theoretical possibility of generalising to other kinds of replicators
such as memes (or something ‘epigenetic’ that Eva Jablonka might be able
to explain but I wouldn’t), in which case my ‘no’ answer might be softened.
But it is enough of a problem already, getting my more hard-headed scientific
colleagues to accept the extended phenotype, without arousing their active
hostility by mentioning memes (which many see as simplistic) or ‘epigenetic
378
inheritance systems’ (which some might write off as obscurantist). I shall
return to the important point, which I enthusiastically accept, that replicators
do not have to be made of DNA in order for the logic of Darwinism to work.
Laland speaks, I suspect, for all three authors when he espouses cyclical
causation. He quotes me as saying
There are causal arrows leading from genes to body. But there is no
causal arrow leading from body to genes.
Laland, who disagrees, generously wants to absolve me from responsibility
for this, saying that he is quoting out of context. But I am happy to stand
by it. ‘Cyclical causation’ leaves me cold. I must, however, make very clear
that I mean causation statistically. Experimentally induced changes in bodies
are never correlated with changes in genes, but changes in genes (mutations) are sometimes correlated with changes in bodies (and all evolution
is the consequence). Of course most mutations occur naturally rather than
experimentally, but (because corrrelation can’t establish causation) I need to
focus on ‘experimentally induced’ in order to pin down the direction of the
causal arrow. It is in this statistical sense that development’s arrow goes only
one way. Attempts to argue for a reverse arrow recur through the history of
biology, and always fail except in unimportant special-pleading senses.
Sterelny, Smith and Dickerson (1996), follow Griffiths and Gray in saying
“Most acorns rot, so acorn genomes correlate better with rotting than with
growth”. But this is dead wrong. It misunderstands the very meaning of
correlation which is, after all, a statistical technical term. Admitting that
most genomes rot, the relevant question is whether such variation as there
may be in acorn genomes correlates with such variation as there may be
in tendency to rot. It probably does, but that isn’t the point. The point is
that the question of covariance is the right question to ask. Sterelny and
Kitcher (1988) in their excellent paper on ‘The Return of the Gene’ are very
clear on the matter. Think variation. Variation, variation, variation. Heritable
variation; covariation between phenotype as dependent variable, and putative
replicator as independent variable. This has been my leitmotif as I read all
three commentators, and it will be my refrain throughout my reply.
Laland’s main contribution to our debate is ‘niche construction’. The
problem I have with niche construction is that it confuses two very different
impacts that organisms might have on their environments. As Sterelny (2000)
put it,
Some of these impacts are mere effects; they are byproducts of the
organisms’s way of life. But sometimes we should see the impact of
organism on environment as the organism engineering its own environment: the environment is altered in ways that are adaptive for the
engineering organism.
379
Niche construction is a suitable name only for the second of these two (and
it is a special case of the extended phenotype). There is a temptation, which
I regard as little short of pernicious, to invoke it for the first (byproducts) as
well. Let’s call the first type by the more neutral term, ‘niche changing’, with
none of the adaptive implications of niche construction or – for that matter –
of the extended phenotype.
A beaver dam, and the lake it creates, are true extended phenotypes insofar
as they are adaptations for the benefit of replicators (presumably alleles
but conceivably something else) that statistically have a causal influence
on their construction. What crucially matters (here’s the leitmotif again) is
that variations in replicators have a causal link to variations in dams such
that, over generations, replicators associated with good dams survive in the
replicator pool at the expense of rival replicators associated with bad dams.
Note what a stringent requirement this is. Although it is not necessary that
we should already have evidence for the replicator-phenotype covariance,
extended phenotype language commits us to a can only have come about
through replicator-phenotype covariance. The beaver’s dam is as much an
adaptation as the beaver’s tail. In neither case have we done the necessary
research to show that it results from gene selection. In both, we have strong
plausibility grounds to think it is. The same is not true – would not even be
claimed by Laland and his colleagues – of most of their proposed examples
of niche construction.