The Selfish Gene: Chapter 13 Summary & Analysis

Dawkins thinks that an “uneasy tension” lies at the heart of the gene’s eye view of evolution. On one hand, there is a beguiling picture of genes—immortal coils, or DNA replicators—forming temporary colonies and passing through generations of mortal, throwaway survival machines. On the other hand, there is a coherent sense of each individual as one agent, as one living thing. Dawkins admits that in some chapters he talks about individuals as if they are agents, enacting strategic behaviors to pass on their genes, while in others he presents things from the gene’s “point of view.” He addresses this “paradox” at length in his book The Extended Phenotype. He’s going to offer a short summary of that book here.   

Genes themselves all look alike. Their differences are only made visible by their effects on the embryos they build. These visible “effects” are called phenotypes. The phenotypic effect of one gene might be “green eyes,” or “curly hair,” for example. Natural selection favors genes on the basis of their phenotypic effects.  Darwinians often think of the phenotypic effects as converging in one organism. A gene that makes an individual run faster keeps the individual alive to reproduce, thus benefiting all the genes in that individual. Dawkins rephrases this as “what’s good for one gene is good for all.”

Dawkins wonders what happens when a gene has a phenotypic effect that’s good for the gene, but bad for the body as a whole. In other words, he’s talking about genes that “cheat.” Geneticist James Crow calls these “genes that beat the system.” For example, t-genes in mice make them sterile or die young, but they also exploit the way that genes are allocated to sperm cells. This is called a “segregation disorder.” When t-genes arise through mutation, they’re in 95 percent of the mouse’s sperm cells (instead of half). They usually cause the population to go extinct.

Dawkins characterizes biologists as people who focus on organisms and ask questions like why they group into societies, and so on. But Dawkins believes that, when one thinks about it, there’s no reason to limit phenotypic effects to a particular individual. In fact, “the phenotypic effects of a gene need to be thought of as all the effects it has on the world.” He wonders this means in practical terms. He suggests that phenotypic effects extending beyond the body can be seen in things like beaver dams, bird nests, and caddis houses. After all, these all help the genes survive too. 

When caddis flies are larvae at the bottom of a lake, they meticulously build “mobile homes” out of tiny stones and sticks that they protect themselves with like shells. Natural selection favors caddis larvae that build the best protective homes, since this facilitates their survival and reproduction. Dawkins thinks that if a geneticist were to compare the structures of caddis houses, they would be looking at the phenotypic effects of caddis larvae genes. It makes as much sense to think of genes for “stone hardness” or “stone size” in caddis larvae as it does to think about genes for “green eyes” or “wrinkles in peas.” He thinks his logic is “inescapable.”  

Dawkins thinks about parasites next. Flukes (flatworms) are parasites that live in snails. They secrete chemicals that make snails build thicker shells. This is beneficial to the fluke (which is better protected inside the thicker shell), but costly to the snail (because it spends energy building a thick shell that could be saved for sustenance and reproduction). Dawkins thinks this means the fluke’s genes have a phenotypic effect on the snail’s shell. He thinks this happens with a lot of parasites, and it means that phenotypic effects extend to other living bodies.

If a parasite’s genes are transmitted to a new host by way of the host’s reproductive cells, the parasite will do everything it can to keep the host alive and reproducing. Dawkins says, “over evolutionary time it will cease to be a parasite, will cooperate with the host, and may eventually merge into the host’s tissues and become unrecognizable as a parasite at all.”

Parasitic bacteria that live in ambrosia beetles seem so essential to the beetle’s reproductive processes that’s hard to consider them parasitic. Like ants and bees, if a beetle egg is unfertilized it will develop into a male embryo. But unlike ants and bees, beetle eggs need to be “pricked” by something to develop into an embryo at all. Parasitic bacteria do the “pricking,” which enables male embryos to develop. In a sense, the bacteria’s own bodies disappear and merge with the host’s bodies. 

This also happens with sea anemones and algae, and with minute, free-floating DNA fragments called “viroids” or “plasmids” that splice themselves seamlessly into chromosomes in human reproductive cells (and then splice themselves out again in the embryo that’s created). Similarly, venereal disease genes benefit from having their hosts copulate, because this allows the gene to spread and replicate in a new host. In fact, they even benefit from having attractive hosts (which makes copulation more likely).

According to Dawkins, phenotypic effects can extend as far as across entire lakes (for example, in beaver dams), and that parasites can influence hosts from afar as well. For example, cuckoos who hatch in other birds’ nests (such as songbird nests) are technically parasites. Dawkins thinks the idea of an organism having its “own body” is a “loaded assumption,” because phenotypic effects can extend far beyond an organism’s “own body” and external parasites (like cuckoos) can manipulate a host’s behavior as much as internal ones can.

For example, some parasitic ants invade a nest, kill the queen (either by slowly severing her head, or more efficiently, secreting a chemical that makes the workers do it), and take her place, while the unwitting worker ants tend to the parasite’s brood. Similarly, some cocooned caterpillars emit noises, which make ants attach onto their cocoons and fend off predators. Dawkins thinks it doesn’t make sense to talk about individuals and others. One should only be talking about genes and phenotypic effects. His central claim about extended phenotypes is that “an animal’s behavior tends to maximize the survival of the genes ‘for’ that behavior, whether or not those genes happen to be in the body of the particular animal performing it.”

Dawkins suggests that one way to get around the problem of talking about “individuals” is to talk about replicators and vehicles. The fundamental units of evolution are things that replicate. In humans, this is DNA. They “gang together” in communal survival machines, or vehicles. In humans, these vehicles are our bodies. Replicators don’t run around and escape from predators, they make their vehicles do that. Vehicles don’t replicate, they facilitate the propagation of replicators. He thinks biologists focus on the “vehicle,” but they should be focusing on the “replicator.”

For Dawkins, “organism” and “group of organisms” are candidates for the “vehicle” role, but neither are candidates for the “replicator” role. Between individuals and groups, “individuals” win out as vehicles, because the category “group” is too “wishy-washy.” The unity of an individual lion far surpasses the unity of a pride of lions.

The Extended Phenotype attempts to answer questions about why genes gang up in cells, live in survival machines, and transfer to new hosts via a “bottleneck” route of reproduction. Dawkins briefly sketches out some of those answers here.  

Cells, to Dawkins, are like pharmaceutical factories. DNA molecules make proteins that work as enzymes (they cause chemical reactions). Each gene makes one type of enzyme. But sometimes multiple enzymes are needed to make a useful product. So, a cell is like a production line that makes an end-product through a series of intermediate steps. Cells essentially keep the genes that cooperate together. However, the cooperating genes aren’t selected as a “group.” They come together by chance, and if their combination doesn’t produce a viable end product, the cell dies. At the bottom of all this behavior is still a single selfish gene that benefits from cooperation with other genes.

Dawkins wonders next why cells clump together into bodies or “lumbering robots.” He remembers that each cell is a clone containing all the genes in the whole body. He decides that cells that club together can “specialize.” Some of them can focus on watching for predators, others can focus on digesting food, and so on. This means that different genes are “turned on” in different cells. The genes that are turned on in one cell benefit their copies that are dormant in other cells.

Finally, Dawkins wonders why genes propagate through the “bottleneck” route of reproduction. It doesn’t matter how big or complex an organism is— each time, the next generation begins with a new single cell, a fertilized egg. He thinks this is like “going back to the drawing board.” Genes don’t take an existing heart and remodel it into a new one—they grow new ones “inspired” by the previous model. The “growth cycle” of an embryo (including birth and childhood) also allows certain genes to be turned on at certain points in the growth cycle. Dawkins thinks this is necessary for precise and complex organs like bird’s wings or eagle’s eyes to be created. He calls this an “orderly timing cycle.”

The third reason for a bottleneck life cycle is “cellular uniformity.” Evolution happens through cell mutation. Imagine there’s a plant called “splurge-weed” that reproduces by shedding a branch that grows another body. A mutant gene would have to spread one by one into all the cells of the splurge weed before the next shedding happened. But if a mutant gene arises in a single cell that clones itself to make a new body (say, in another imaginary plant called “bottle-wrack”) it’s already automatically going to be in every cell of the embryo that’s built. It’s also more likely the cells in that survival machine will cooperate, since they have the same interest at heart: propagation of the genes inside them. Dawkins thinks the evolutionary payoff of a “bottleneck” reproductive cycle is why there are discrete organisms at all. 

There’s a lot more to The Extended Phenotype, but Dawkins hopes he’s given a “flavor” of the book here. He concludes by giving a “brief manifesto” of the “selfish gene/extended phenotype” view of life, which he thinks applies to all living beings, everywhere in the universe. The manifesto begins with the claim that “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 by chance, but once they exist, they can make infinite copies of themselves.  

Since no copying process is perfect, slightly different replicators will emerge that are better or worse at making copies of themselves. The ones that are best at making copies of themselves “come to dominate the population.” Over time, “the world becomes filled with the most powerful and ingenious replicators.” 

Replicators will find more and more elaborate ways of perpetuating themselves. Replicators survive because of their “consequences on the world.” These can be quite indirect, but as long as they affect the replicator’s success at getting copied, they still count. The success of a replicator depends on the world it’s placed in. One of the most important factors is other replicators. Just like the oarsmen, replicators that work well together to achieve a joint goal will dominate the world.    

At some point in time, this “ganging up of mutually compatible replicators” formalized into discrete vehicles: “cells, and later, many celled bodies.” The vehicles that evolved a “bottleneck” life cycle prospered. This made them more “discrete” and “vehicle-like.” This “packaging of living material into discrete vehicles” became so visible that, when biologists started inquiring about the world around them, “their questions were mostly about vehicles—individual organisms.” Dawkins thinks that biology needs to be turned “the right way up” by realizing that replicators came first. He suggests that one way to do this is to remember that phenotypic effects of a gene are not limited to the body it lives in.       

If one use one’s imagination, one can see the gene as “sitting at the centre of a radiating web of extended phenotypic power.”  Similarly, one can imagine every object in the world sitting at the center of several converging webs of influences from many genes sitting in many organisms. The world is “criss-crossed” with arrows joining phenotypic effects to genes. Dawkins concludes that replicators are no longer peppered freely around the universe. They are packaged into individual bodies. Similarly, many phenotypic effects have “congealed” into those bodies instead of being spread evenly throughout the world. But the “individual body” did not have to exist. The only kind of entity that has to exist for life to arise is the immortal replicator.