Darwin’s ‘survival of the fittest’ is really a special case of a more general law of survival of the stable. The universe is populated by stable things. […] But when the replicators became numerous, building blocks must have been used up at such a rate that they became a scarce and precious resource. […] Some of them may even have ‘discovered’ how to break up molecules of rival varieties chemically, and to use the building blocks so released for making their own copies. These proto-carnivores simultaneously obtained food and removed competing rivals. Other replicators perhaps discovered how to protect themselves, either chemically, or by building a physical wall of protein around themselves. This may have been how the first living cells appeared. Replicators began not merely to exist, but to construct for themselves containers, vehicles for their continued existence. The replicators that survived were the ones that built survival machines for themselves to live in. […]

A society of ants, bees, or termites achieves a kind of individuality at a higher level. Food is shared to such an extent that one may speak of a communal stomach. Information is shared so efficiently by chemical signals and by the famous ‘dance’ of the bees that the community behaves almost as if it were a unit with a nervous system and sense organs of its own. Foreign intruders are recognized and repelled with something of the selectivity of a body’s immune reaction system. The rather high temperature inside a beehive is regulated nearly as precisely as that of the human body, even though an individual bee is not a ‘warm blooded’ animal. Finally and most importantly, the analogy extends to reproduction. The majority of individuals in a social insect colony are sterile workers. The ‘germ line’—the line of immortal gene continuity—flows through the bodies of a minority of individuals, the reproductives. These are the analogues of our own reproductive cells in our testes and ovaries. The sterile workers are the analogy of our liver, muscle, and nerve cells. […]

I think that a new kind of replicator has recently emerged on this very planet. It is staring us in the face. It is still in its infancy, still drifting clumsily about in its primeval soup, but already it is achieving evolutionary change at a rate that leaves the old gene panting far behind. The new soup is the soup of human culture. We need a name for the new replicator, a noun that conveys the idea of a unit of cultural transmission, or a unit of imitation. ‘Mimeme’ comes from a suitable Greek root, but I want a monosyllable that sounds a bit like ‘gene’. I hope my classicist friends will forgive me if I abbreviate mimeme to meme.*


The word meme seems to be turning out to be a good meme. It is now quite widely used and in 1988 it joined the official list of words being considered for future editions of Oxford English Dictionaries. This makes me the more anxious to repeat that my designs on human culture were modest almost to vanishing point. My true ambitions—and they are admittedly large—lead in another direction entirely. I want to claim almost limitless power for slightly inaccurate self-replicating entities, once they arise anywhere in the universe. This is because they tend to become the basis for Darwinian selection which, given enough generations, cumulatively builds systems of great complexity. I believe that, given the right conditions, replicators automatically band together to create systems, or machines, that carry them around and work to favour their continued replication. The first ten chapters of The Selfish Gene had concentrated exclusively on one kind of replicator, the gene. In discussing memes in the final chapter I was trying to make the case for replicators in general, and to show that genes were not the only members of that important class. Whether the milieu of human culture really does have what it takes to get a form of Darwinism going, I am not sure. But in any case that question is subsidiary to my concern. Chapter 11 will have succeeded if the reader closes the book with the feeling that DNA molecules are not the only entities that might form the basis for Darwinian evolution. My purpose was to cut the gene down to size, rather than to sculpt a grand theory of human culture.

Fundamentally, the reason why it is good policy for us to try to explain biological phenomena in terms of gene advantage is that genes are replicators. As soon as the primeval soup provided conditions in which molecules could make copies of themselves, the replicators themselves took over. For more than three thousand million years, DNA has been the only replicator worth talking about in the world. But it does not necessarily hold these monopoly rights for all time. Whenever conditions arise in which a new kind of replicator can make copies of itself, the new replicators will tend to take over, and start a new kind of evolution of their own. Once this new evolution begins, it will in no necessary sense be subservient to the old. The old gene-selected evolution, by making brains, provided the soup’ in which the first memes arose. Once self-copying memes had arisen, their own, much faster, kind of evolution took off.

What if a mutant gene arose that just happened to have an effect, not upon something obvious like eye colour or curliness of hair, but upon meiosis itself? Suppose it happened to bias meiosis in such a way that it, the mutant gene itself, was more likely than its allelic partner to end up in the egg. There are such genes and they are called segregation distorters. They have a diabolical simplicity. When a segregation distorter arises by mutation, it will spread inexorably through the population at the expense of its allele. It is this that is known as meiotic drive. It will happen even if the effects on bodily welfare, and on the welfare of all the other genes in the body, are disastrous. […]

The individual organism is something whose existence most biologists take for granted, probably because its parts do pull together in such a united and integrated way. Questions about life are conventionally questions about organisms. Biologists ask why organisms do this, why organisms do that. They frequently ask why organisms group themselves into societies. They don’t ask—though they should—why living matter groups itself into organisms in the first place. Why isn’t the sea still a primordial battleground of free and independent replicators? Why did the ancient replicators club together to make, and reside in, lumbering robots, and why are those robots—individual bodies, you and me—so large and so complicated? […]

The phenotypic effects of a gene are normally seen as all the effects that it has on the body in which it sits. This is the conventional definition. But we shall now see that the phenotypic effects of a gene need to be thought of as all the effects that it has on the world. It may be that a gene’s effects, as a matter of fact, turn out to be confined to the succession of bodies in which the gene sits. But, if so, it will be just as a matter of fact. It will not be something that ought to be part of our very definition. In all this, remember that the phenotypic effects of a gene are the tools by which it levers itself into the next generation. All that I am going to add is that the tools may reach outside the individual body wall. What might it mean in practice to speak of a gene as having an extended phenotypic effect on the world outside the body in which it sits? Examples that spring to mind are artefacts like beaver dams, bird nests and caddis houses. […] [C]addis larvae are anything but nondescript. They are among the most remarkable creatures on earth. Using cement of their own manufacture, they skilfully build tubular houses for themselves out of materials that they pick up from the bed of the stream. The house is a mobile home, carried about as the caddis walks, like the shell of a snail or hermit crab except that the animal builds it instead of growing it or finding it. Some species of caddis use sticks as building materials, others fragments of dead leaves, others small snail shells. But perhaps the most impressive caddis houses are the ones built in local stone. The caddis chooses its stones carefully, rejecting those that are too large or too small for the current gap in the wall, even rotating each stone until it achieves the snuggest fit. Incidentally, why does this impress us so? If we forced ourselves to think in a detached way we surely ought to be more impressed by the architecture of the caddis’s eye, or of its elbow joint, than by the comparatively modest architecture of its stone house. After all, the eye and the elbow joint are far more complicated and ‘designed’ than the house. Yet, perhaps because the eye and elbow joint develop in the same kind of way as our own eyes and elbows develop, a building process for which we, inside our mothers, claim no credit, we are illogically more impressed by the house. […]

Although geneticists may think it an odd idea, it is therefore sensible for us to speak of genes ‘for’ stone shape, stone size, stone hardness and so on. […] A geneticist might wish to claim that the direct influence of the genes is upon the nervous system that mediates the stone-choosing behaviour, not upon the stones themselves. But I invite such a geneticist to look carefully at what it can ever mean to speak of genes exerting an influence on a nervous system. All that genes can really influence directly is protein synthesis. […]

To quite a large extent the interests of parasite genes and host genes may coincide. From the selfish gene point of view we can think of both fluke genes and snail genes as ‘parasites’ in the snail body. Both gain from being surrounded by the same protective shell, though they diverge from one another in the precise thickness of shell that they ‘prefer’. This divergence arises, fundamentally, from the fact that their method of leaving this snail’s body and entering another one is different. For the snail genes the method of leaving is via snail sperms or eggs. For the fluke’s genes it is very different. Without going into the details (they are distractingly complicated) what matters is that their genes do not leave the snail’s body in the snail’s sperms or eggs. […]

Wood-boring ambrosia beetles (of the species Xyleborus ferrugineus) are parasitized by bacteria that not only live in their host’s body but also use the host’s eggs as their transport into a new host. The genes of such parasites therefore stand to gain from almost exactly the same future circumstances as the genes of their host. The two sets of genes can be expected to ‘pull together’ for just the same reasons as all the genes of one individual organism normally pull together. It is irrelevant that some of them happen to be ‘beetle genes’, while others happen to be ‘bacterial genes’. Both sets of genes are ‘interested’ in beetle survival and the propagation of beetle eggs, because both ‘see’ beetle eggs as their passport to the future. So the bacterial genes share a common destiny with their host’s genes, and in my interpretation we should expect the bacteria to cooperate with their beetles in all aspects of life. It turns out that ‘cooperate’ is putting it mildly. The service they perform for the beetles could hardly be more intimate. These beetles happen to be haplodiploid, like bees and ants (see Chapter 10). If an egg is fertilized by a male, it always develops into a female. An unfertilized egg develops into a male. Males, in other words, have no father. The eggs that give rise to them develop spontaneously, without being penetrated by a sperm. But, unlike the eggs of bees and ants, ambrosia beetle eggs do need to be penetrated by something. This is where the bacteria come in. They prick the unfertilized eggs into action, provoking them to develop into male beetles. […]

We can take this argument to its logical conclusion and apply it to normal, ‘own’ genes. Our own genes cooperate with one another, not because they are our own but because they share the same outlet—sperm or egg—into the future. If any genes of an organism, such as a human, could discover a way of spreading themselves that did not depend on the conventional sperm or egg route, they would take it and be less cooperative. This is because they would stand to gain by a different set of future outcomes from the other genes in the body. […]

Beaver lakes are extended phenotypic effects of beaver genes, and they can extend over several hundreds of yards. A long reach indeed![…]

The group of organisms—the flock of birds, the pack of wolves—does not merge into a single vehicle, precisely because the genes in the flock or the pack do not share a common method of leaving the present vehicle. To be sure, packs may bud off daughter packs. But the genes in the parent pack don’t pass to the daughter pack in a single vessel in which all have an equal share. The genes in a pack of wolves don’t all stand to gain from the same set of events in the future. A gene can foster its own future welfare by favouring its own individual wolf, at the expense of other individual wolves. An individual wolf, therefore, is a vehicle worthy of the name. A pack of wolves is not. Genetically speaking, the reason for this is that all the cells except the sex cells in a wolf’s body have the same genes, while, as for the sex cells, all the genes have an equal chance of being in each one of them. But the cells in a pack of wolves do not have the same genes, nor do they have the same chance of being in the cells of sub-packs that are budded off. […]

Everywhere we find that life, as a matter of fact, is bundled into discrete, individually purposeful vehicles like wolves and bee-hives. But the doctrine of the extended phenotype has taught us that it needn’t have been so. Fundamentally, all that we have a right to expect from our theory is a battleground of replicators, jostling, jockeying, fighting for a future in the genetic hereafter. The weapons in the fight are phenotypic effects, initially direct chemical effects in cells but eventually feathers and fangs and even more remote effects. It undeniably happens to be the case that these phenotypic effects have largely become bundled up into discrete vehicles, each with its genes disciplined and ordered by the prospect of a shared bottleneck of sperms or eggs funnelling them into the future. But this is not a fact to be taken for granted. It is a fact to be questioned and wondered at in its own right. Why did genes come together into large vehicles, each with a single genetic exit route? Why did genes choose to gang up and make large bodies for themselves to live in? In The Extended Phenotype I attempt to work out an answer to this difficult problem. […]

I shall divide the question up into three. Why did genes gang up in cells? Why did cells gang up in many-celled bodies? And why did bodies adopt what I shall call a ‘bottlenecked’ life cycle? […]

And no matter how many cells, of no matter how many specialized types, cooperate to perform the unimaginably complicated task of running an adult elephant, the efforts of all those cells converge on the final goal of producing single cells again—sperms or eggs. The elephant not only has its beginning in a single cell, a fertilized egg. Its end, meaning its goal or end-product, is the production of single cells, fertilized eggs of the next generation. The life cycle of the broad and bulky elephant both begins and ends with a narrow bottleneck. This bottlenecking is characteristic of the life cycles of all many-celled animals and most plants. Why? What is its significance? We cannot answer this without considering what life might look like without it. It will be helpful to imagine two hypothetical species of seaweed called bottle-wrack and splurge-weed. Splurge-weed grows as a set of straggling, amorphous branches in the sea. Every now and then branches break off and drift away. These breakages can occur anywhere in the plants, and the fragments can be large or small. As with cuttings in a garden, they are capable of growing just like the original plant. This shedding of parts is the species’s method of reproducing. As you will notice, it isn’t really different from its method of growing, except that the growing parts become physically detached from one another. Bottle-wrack looks the same and grows in the same straggly way. There is one crucial difference, however. It reproduces by releasing single-celled spores which drift off in the sea and grow into new plants. These spores are just cells of the plant like any others. As in the case of splurge-weed, no sex is involved. The daughters of a plant consist of cells that are clone-mates of the cells of the parent plant. The only difference between the two species is that splurgeweed reproduces by hiving off chunks of itself consisting of indeterminate numbers of cells, while bottle-wrack reproduces by hiving off chunks of itself always consisting of single cells. […]

There is only a limited amount of change that can be achieved by direct transformation in the ‘swords to ploughshares’ manner. Really radical change can be achieved only by going ‘back to the drawing board’, throwing away the previous design and starting afresh. When engineers go back to the drawing board and create a new design, they do not necessarily throw away the ideas from the old design. But they don’t literally try to deform the old physical object into the new one. The old object is too weighed down with the clutter of history. Maybe you can beat a sword into a ploughshare, but try ‘beating’ a propellor engine into a jet engine! You can’t do it. You have to discard the propellor engine and go back to the drawing board. Living things, of course, were never designed on drawing boards. But they do go back to fresh beginnings. They make a clean start in every generation. Every new organism begins as a single cell and grows anew. […]

With mutations around, the cells within a plant of splurge-weed will not have all the same genetic interests at heart. A gene in a splurge-weed cell stands to gain by promoting the reproduction of its cell. It does not necessarily stand to gain by promoting the reproduction of its ‘individual’ plant. Mutation will make it unlikely that the cells within a plant are genetically identical, so they won’t collaborate wholeheartedly with one another in the manufacture of organs and new plants. Natural selection will choose among cells rather than ‘plants’. In bottle-wrack, on the other hand, all the cells within a plant are likely to have the same genes, because only very recent mutations could divide them. Therefore they will happily collaborate in manufacturing efficient survival machines. Cells in different plants are more likely to have different genes. After all, cells that have passed through different bottlenecks may be distinguished by all but the most recent mutations—and this means the majority. Selection will therefore judge rival plants, not rival cells as in splurge-weed. So we can expect to see the evolution of organs and contrivances that serve the whole plant. […]

We can think of an individual organism as a ‘group’ of cells. A form of group selection can be made to work, provided some means can be found for increasing the ratio of between-group variation to within-group variation. Bottle-wrack’s reproductive habit has exactly the effect of increasing this ratio; splurge-weed’s habit has just the opposite effect. […]

Let me end with a brief manifesto, a summary of the entire selfish gene/extended phenotype view of life. It is a view, I maintain, that applies to living things everywhere in the universe. The fundamental unit, the prime mover of all life, is the replicator. A replicator is anything in the universe of which copies are made. Replicators come into existence, in the first place, by chance, by the random jostling of smaller particles. Once a replicator has come into existence it is capable of generating an indefinitely large set of copies of itself. No copying process is perfect, however, and the population of replicators comes to include varieties that differ from one another. Some of these varieties turn out to have lost the power of self-replication, and their kind ceases to exist when they themselves cease to exist. Others can still replicate, but less effectively. Yet other varieties happen to find themselves in possession of new tricks: they turn out to be even better self-replicators than their predecessors and contemporaries. It is their descendants that come to dominate the population. As time goes by, the world becomes filled with the most powerful and ingenious replicators. Gradually, more and more elaborate ways of being a good replicator are discovered. Replicators survive, not only by virtue of their own intrinsic properties, but by virtue of their consequences on the world. These consequences can be quite indirect. All that is necessary is that eventually the consequences, however tortuous and indirect, feed back and affect the success of the replicator at getting itself copied. The success that a replicator has in the world will depend on what kind of a world it is—the pre-existing conditions. Among the most important of these conditions will be other replicators and their consequences. Like the English and German rowers, replicators that are mutually beneficial will come to predominate in each other’s presence. At some point in the evolution of life on our earth, this ganging up of mutually compatible replicators began to be formalized in the creation of discrete vehicles—cells and, later, many-celled bodies. Vehicles that evolved a bottlenecked life cycle prospered, and became more discrete and vehicle-like. This packaging of living material into discrete vehicles became such a salient and dominant feature that, when biologists arrived on the scene and started asking questions about life, their questions were mostly about vehicles—individual organisms. The individual organism came first in the biologist’s consciousness, while the replicators—now known as genes—were seen as part of the machinery used by individual organisms. It requires a deliberate mental effort to turn biology the right way up again, and remind ourselves that the replicators come first, in importance as well as in history. One way to remind ourselves is to reflect that, even today, not all the phenotypic effects of a gene are bound up in the individual body in which it sits. Certainly in principle, and also in fact, the gene reaches out through the individual body wall and manipulates objects in the world outside, some of them inanimate, some of them other living beings, some of them a long way away. With only a little imagination we can see the gene as sitting at the centre of a radiating web of extended phenotypic power. And an object in the world is the centre of a converging web of influences from many genes sitting in many organisms. The long reach of the gene knows no obvious boundaries. The whole world is criss-crossed with causal arrows joining genes to phenotypic effects, far and near. It is an additional fact, too important in practice to be called incidental but not necessary enough in theory to be called inevitable, that these causal arrows have become bundled up. Replicators are no longer peppered freely through the sea; they are packaged in huge colonies—individual bodies. And phenotypic consequences, instead of being evenly distributed throughout the world, have in many cases congealed into those same bodies. But the individual body, so familiar to us on our planet, did not have to exist. The only kind of entity that has to exist in order for life to arise, anywhere in the universe, is the immortal replicator.

Richard Dawkins, The Selfish Gene, 30th Anniversary Edition, 2006

Footnotes (1989 edition) are doubly indented.

Added to diary 27 June 2018