#extended phenotype

[joibittle]

What the spider sees...Back in the studio after CUNY graduation last spring (2025) - a new octet rule. Please visit my studio blog page here. https://joibittlestudio.tumblr.com/

[astranemus]

In the case of Ophiocordyceps, an infected ant's behaviour car be thought of as fungal behaviour. The death grip, summit disease, these are extended characteristics of the fungus, part of its extended phenotype. Can the alterations in human consciousness and behaviour brought about by psilocybin mushrooms be thought of as part of the extended phenotype of the fungus? The extended behaviour of Ophiocordyceps leaves an imprint in the world in the form of fossilised scars on the underside of leaves. Can the extended behaviour of psilocybin mushrooms be thought of as leaving an imprint in the world in the form of ceremonies, rituals, chants and the other cultural and technological outgrowths of our altered states? Do psilocybin fungi wear our minds, as Ophiocordyceps and Massospora wear insect bodies?

Terence McKenna was a great advocate of this view. Given a sufficiently large dose, he asserted, the mushroom could de expected to speak, plainly and clearly, talking 'eloquently of itself in the cool night of the mind'. Fungi have no hands with which to manipulate the world but with psilocybin as a chemical messenger, they could borrow a human body, and use its brain and senses to think and speak through. McKenna thought fungi could wear our minds, occupy our senses and, most important, impart knowledge about the world out there. Among other things, fungi could use psilocybin to influence humans in an attempt to deflect our destructive habits as a species. For McKenna, this was a symbiotic partnership that presented possibilities 'richer and even more baroque' than those available to humans or fungi alone.

As Dawkins reminds us, how far we're willing to go depends on how far we're willing to speculate. How we speculate in turn depends on how we arrange our biases. 'You think the world is what it looks like in fine weather at noon day,' the philosopher Alfred North Whitehead once observed to his former student Bertrand Russell. 'I think it is what it seems like in the early morning when one first wakes from deep sleep.' In Whitehead's terms, Dawkins speculates in fine weather at noon day. He takes pains to ensure that his speculation about extended phenotypes remains 'disciplined' and 'tightly limited'. He is clear that phenotypes can extend beyond the body, but they can't be too extended. By contrast, McKenna speculates at dawn. His requirements are less stringent, his explanations less tightly limited. Between the two poles lies a continent of possible opinion.

Merlin Sheldrake, Entangled Life: How Fungi Make Our Worlds, Change Our Minds, And Shape Our Futures

[religion-is-a-mental-illness]

Is the Blue Mosque an extended phenotype?

I enjoy fielding questions after a public lecture.

By: Richard Dawkins

Published: Sep 25, 2025

I enjoy fielding questions after a public lecture. Sometimes a question merits a single yes or no answer. Once, at the Hay-on-Wye Literary Festival, I was privileged to hear Stephen Hawking lecture. Because of his disability, he was obliged to record his lecture in advance, including answers to questions previously submitted. At the end, however, the chairman announced that, as a rare concession, Professor Hawking would entertain one spontaneous question. Who would like to ask it? A gentleman was chosen.

“Professor Hawking, would you not agree that there is a spiritual dimension to the universe, a transcendent, immanent mysterium, going apophatically beyond mere physics and chemistry . . .” and so on and on, at obscurantist, meaningless length. Hawking settled down to answer the question, twitching his functioning muscle, building his answer up letter by letter, phoneme by phoneme, while we, the audience, waited with bated breath for the oracle to pronounce. Fully ten minutes later, his answer was assembled, and the famous robotic voice echoed through the auditorium.

“No!”

A man with a sense of humour.

Other questions go to the opposite extreme. Far from inviting a one-word answer, they require what amounts to a small lecture explaining to the audience the meaning of the question. One such question – an extremely common and good question – is the following: “ Is this auditorium an extended phenotype?” The correct answer is again a decisive No.

From my hotel in Istanbul as I write, I have a good view of the Blue Mosque, one of the world’s great feats of architecture, and also of the older and perhaps even more splendid Hagia Sophia, originally a Byzantine cathedral, then a mosque, then a museum, and now a mosque again. The common “auditorium” question could even more appositely be asked of either of these magnificent buildings, and the answer is still no. They are not extended phenotypes. Let me explain.

An organism’s “phenotype” is its observable characteristics, but the word is often reserved for the manifestation of a genotype. The “selfish gene” view of neo-Darwinism sees the phenotype as the observable instrument by which a gene levers itself into the next generation. A bird’s wing is just such an instrument. It has the proximal effect of levering the bird into the air, which contributes to the ultimate effect of levering the bird’s genes into the next generation. Especially (this is what really matters) the genes responsible for shaping the wing’s aerodynamic efficiency. I chose a bird wing by way of example, but the same argument applies to every bit of the phenotype of every organism that ever lived.

That’s “phenotype” in the conventional sense. Phenotypic characteristics, as normally understood, are parts of an animal’s body: a wing, a tail, an ornamental crest. An extended phenotype is not a part of the animal’s body, but it plays the same Darwinian role. A typical example is a bird’s nest. It’s made of dead twigs and grass, but it is shaped in such a way as to preserve and assist the passing on of the bird’s genes. Genes in the bird influence the shape of the nest via the bird’s behaviour, affecting the nest’s efficiency in its task of keeping the eggs safe and warm: eggs that contain the very same genes that influenced the shape of the nest. These particular pendant nests, built by weaver birds, are probably adapted additionally to be safe from snakes.

The proximal route by which the genes affect the nest’s shape is the building behaviour performed by the bird. A gene that slightly changed the building behaviour with the result that eggs were more likely to fall out of the nest is less likely to survive into the next generation. The same is true of a gene whose effect on building behaviour is to alter the lining of the nest such that the eggs are too cold. The details can easily be imagined, along with their opposites for genes with high survival value. The point is that, one way or another, genes influence nests in ways that affect their own – the genes’ own – survival. Mutations in bird genes manifest themselves as changes in nests, and hence affect their own survival. You could do a genetic study of weaver bird nests, no less than a genetic study of peas in a monastery garden. Nests are extended phenotypes. So are beaver dams. So are bower bird bowers.

So are termite mounds, even though the genes concerned sit in thousands of sterile workers rather than a pair of fertile weaver birds.

The late Daniel Dennett compared the above two magnificent buildings, the one designed by Antoni Gaudi and built by large numbers of men from Barcelona, the other never designed but nevertheless built, by a much larger workforce of termites from Australia. The one on the left is an extended phenotype of termite genes. But what about the one on the right? Shouldn’t we, by analogy, consider it the extended phenotype of Antoni Gaudi’s genes? No.

Or what about Istanbul ‘s Blue Mosque, which filled me with awe when I joined the seething crowds to visit it yesterday? Is that not the extended phenotype of the genes of Sedefkar Mehmet Aga (1562-1617). No. Again, the answer is no, and it is my purpose here to explain why.

The reason is not that the architect was one man and the termites many. Nor is it that the mosque was designed (“top down”) whereas the termite mound self-assembled (“bottom up”), an interesting but irrelevant distinction. It’s because there are no genes for different architectural styles. At least, I assume there aren’t. There may conceivably be genes for being a good architect, which might also be described as genes for artistic flair, or even for something as specific as a good sense of proportion. But (I conjecture) there are no genes for blue domes, no genes for soaring minarets, no genes for cunningly interlaced arches.

I don’t absolutely know that there are genes for nest shape in weaver birds. To prove it, I’d need to do breeding experiments, systematically choosing to breed from birds whose nest was a particular shape – perhaps a deeper cup below the entrance hole, or perhaps a smaller entrance hole. The experiment has not been done, but I’m confident of the result. Why? Because the nest is obviously an evolutionary consequence of Darwinian natural selection, and natural selection can’t have evolutionary consequences unless there are genetic variants to choose among. In order for weaver bird nests to have evolved their egg-warming and chick-protecting shape, there must have been genes for variation in nest attributes. The nest is an extended phenotype of bird genes. Nobody has done the experiment of systematically breeding architects for many generations, and I can’t be totally sure that you wouldn’t succeed in breeding a race of architects with an inborn penchant for blue domes, but my strong doubts embolden me to move on to a new point.

A church or mosque may not be an extended phenotype of genes, but what about memes? Darwinian selection is the differential survival of replicators, defined as entities, of which exact (and occasionally inexact) copies are made. Life on Earth is almost exclusively the product of the differential survival of DNA-coded genes in gene pools. But genes are not the only conceivable replicators. Memes, units of cultural inheritance, are also replicators, and are also potentially subject to a form of natural selection. There are no (or so I believe) genes for blue domes. But there could well be memes for blue domes. Architects influence each other. They inherit memes from other architects. Styles of ecclesiastical architecture evolve as the decades and centuries go by. We give them names: baroque, rococo, neo-classical, Romanesque, byzantine, Bauhaus, brutalist, postmodern. Architects pick up ideas from already constructed buildings and copy them, perhaps with modifications. Churches, mosques, buildings generally, are phenotypes not of genes but of memes.

But isn’t it absurdly reductionist (whatever that means) to see evolving architectural styles as the natural selection of replicators? What about the human architects whose free choice it is to adopt one style or another? Well, yes, that’s another and a defensible way to look at it. But the memetic way is compatible with it. The mentality of architects, their upbringing, education, parental influence, even their genes, constitute an ecosystem in which a meme may flourish or die. The architecture that we see in any century is a result of a winnowing of memes that took place in the context of that ecosystem. And, by the way, architectural memes in particular run a more serious gauntlet than that of future architects’ imitative taste. How many buildings are, like the Blue Mosque, still standing (and in a position to be imitated) after 415 years? Hagia Sophia is not only in excellent repair after nearly 1500 years. It has projected down the centuries the memes of two rival, mutually persecuting, mutually intolerant and belligerent religions – and still stands. A great cathedral or mosque is the phenotype (no need to call it “extended”) of a meme complex, a memeplex of naturally selected architectural replicators, standing through the centuries and silently – via the eyes, brains and hands of architects – throwing off stylish memes to be inherited by lesser and more transient buildings.

[whathofstadterdoesntsay]

ZOMBIE SNAIL

[autismandhumanatavism]

In modern evolutionary theory, selection acts on particular genes and assemblages of genes that operate through phenotypes expressed in environments. This view, however, overlooks the fact that organisms often alter their environments in pursuit of fitness needs and thus modify some environmental selection pressures. Niche construction theory introduces a reciprocal causal process that modifies natural selection relative to three general kinds of environmental components: abiota, biota (other organisms), and artifacts. The ways in which niche-constructing organisms can construct or modify the components differ. Modification of abiota, for example, may have different consequences from the construction of artifacts. Some changes in abiota may simply be caused by the by-products of metabolisms and activities of organisms. Alternatively, artifacts may be “extended phenotypes” that demonstrate obvious prior “design” and “construction” by organisms in the service of fitness needs. Nevertheless, adaptation should always account for the reciprocity between constructed niches and the living agents that construct them. Looking to well-adapted nature for inspiration for human-built artifacts must account for this reciprocity between phenotype and constructed environment as well as the novel features of human architecture, including frank intentionality of design and novel culturally acquired knowledge.

Niche Construction Theory and Human Architecture

"Artifact" = Simulacrum?

[autismandhumanatavism]

These results provide a genetic basis for the extended phenotype whereby a gene in one organism (the parasite) has phenotypic effects on another organism (the host).

A Gene for an Extended Phenotype

[jaygrayves-blog]

"People seem to have little difficulty in acception the modifiability of 'environmental' effects on human development. If a child has had bad teaching in mathematics, it is accepted that the resulting deficiency can be remedied by extra good teaching the following year. But any suggestion that the child's mathematical deficiency might have a genetic origin is likely to be greeted with something approaching despaire: if it is in the genes 'it is written,' it is 'determined' and nothing can be done about it: you might as well give up attempting to teach the child mathematics. This is pernicious rubbish on an almost astrological scale. Genetic causes and environmental causes are in principle no different from each other. Some influences of both types may be hard to reverse; others may be easy to reverse. Some may be usually hard to revers but easy if the right agent is applied. The important point is that there is no general reason for expecting genetic influences o be any more irreversible than environmental ones.

What did genes do to deserve their sinister, juggernaut-like reputation?...Why are genes though to be so much more fixed and inescapable in their effects than television, nuns, or books? Don't blame your mates for sleeping around, ladies, it's not their fault they have been inflamed by pornographic literature! The alleged Jesuit boast, 'give me the child for his first seven years, and I'll give you the man,' may have some truth in it. Educational, or other cultural influences may, in some circumstances, be just as unmodifiable and irreversible as genes and 'stars' are popularly thought to be"

The Extended Phenotype by Richard Dawkins