We talk to the renowned evolutionary biologist about "The Genetic Book of the Dead" and how we can read the history of life on Earth through modern genes
In his 1976 debut volume, Richard Dawkins pioneered the concept of the “selfish gene” – the idea that genes propagate themselves through whatever mechanisms necessary, thus explaining phenomena such as cooperation between related organisms. The book is widely considered to be one of the most influential works of popular science in the 20th century. He went on to write extensively on evolution and natural selection over the following decades, including works that used criticism of creationism and intelligent design to argue against the existence of God, such as The Blind Watchmaker.
Through his writing, and his many appearances as a public intellectual, Dawkins has been a key figure in promoting a secular, humanist worldview. His 2006 volume The God Delusion was a catalyst of the New Atheist movement, attacking all the major arguments for religion and challenging readers to think critically about their own beliefs.
Dawkins’ most recent book, The Genetic Book of the Dead, is the culminating panel in his Darwinian tapestry – a climactic exploration of the ways that the interactions between genes and the environment shape the lives of organisms. As he explains it, every living thing is a legacy of the interactions between these forces. The genome, he says, is a palimpsest – a record of past interactions playing out in the present.
By peeling back the layers of this palimpsest, we can discern the history of everything from a microbe to a human being. The battles won by the selfish genes of our ancestors manifest in our phenotypes – our bodies.
New Humanist checked in with Dawkins during “The Final Bow”, his last global tour, to discuss his latest work and the fascinating and sometimes bizarre implications of the genes bequeathed by the dead.
What’s behind the title of your most recent work?
It is a poetic allusion to the Egyptian Books of the Dead, which were buried with the dead to guide them to the afterlife. I think of genes as immortal or semi-immortal; they guide the individual – not to preserve itself, but to preserve them. A living organism, over time, becomes a kind of archive, giving us insight into its ancestral history. The body, behaviour and genes of every living creature can be read as a book.
Why do organisms die of old age?
Genes are [potentially] immortal, but not bodies. Genes mature in their effects at particular times. Most of them have their effects in early embryology, but some of them have their effects later.
Imagine a gene which has the effect of giving you cancer. One gives you cancer when you’re 10, another gives you cancer when you’re 20, 30, 40, 50 or 60. The one that gives you cancer when you’re 60 has every opportunity to reproduce before you get the cancer. One that gives you cancer when you’re 10 is out. The younger a lethal gene exerts its effect, the less likely it is to get passed on to the next generation.
So we [humans] are a kind of dustbin of late-acting lethals. The older we are, the more we are susceptible to the influence of late-acting lethal genes.
How can a genome – the complete set of genes present in a cell or organism – be viewed as a palimpsest, a manuscript on which successive texts have been written?
It’s inevitable, because the genome must be a palimpsest of old and then slightly more recent writings. It’s not the case that any particular date in the past is the crucial one for writing the genome. It’s the whole series of successive times.
Do we know why some genes persist in the genome, even if they are not actually deployed?
It’s a bit analogous to your hard disk: there are lots of vestigial documents that you think have been deleted, but they’re not. Their space has been marked as available for further use but they’re still lurking there. I think that the genome is similar to that.
How can seemingly inefficient “design” be useful in tracing evolutionary history? Could you give us an example?
My favourite is the recurrent laryngeal nerve, which affects swallowing, breathing and speech. It follows a pronounced detour from the vagus nerve to the larynx for historical reasons. Our fish ancestors took the most direct route –they had no necks to speak of, so the path from the vagus nerve to the gills, which later evolved into the larynx and other structures, was short. Then, as the neck lengthened in the evolution of land animals, the marginal cost of each increment in the detour was slight compared to the major cost of changing the embryology, such that the nerve jumped over the aorta and looped back around rather than travelling directly to the larynx, which might seem to be more efficient. This is true even in giraffes, despite the fact that the nerve has to take a several-metre detour before reaching the larynx.
The phenotype encompasses all of an individual’s observable traits. It is produced both by genes and the interaction of genes with the environment. You mention mole crickets in the book. How is the burrow created by the cricket part of its phenotype?
The burrow is clearly a survival device, no less than a part of the cricket’s body. It is a phenotype, but an extended phenotype. There must be “genes for” burrow shape and size, no less than for leg shape and size.
Can the effects of one organism on another organism’s genotype and phenotype – as in the dramatic eyespots on moths and butterflies, which mimic other animals – also be considered part of the extended phenotype?
Not in the case of eye spots, but I have written about animal communication as manipulation. Part of the argument states that the change in the manipulatee’s behaviour can be seen as part of the manipulator’s extended phenotype. For example, when a male canary sings to a female, her ovaries swell, and her hormonal state changes. These changes can be seen as part of the extended phenotype of genes in the male.
There are competing views of adaptation – one that adaptations are “good enough” and another that they are essentially “perfect”. What do you think?
The word “satisficing” is used to mean “sometimes it’s good enough, it doesn’t have to be perfect”. I think the problem with that is that evolution is a competitive business. If you’re just good enough, somebody else is going to be a bit better than good enough. In competition, just good enough will lose out against the one that is a bit better.
But surely adaptations aren’t perfect? For example organisms are encoded to discern patterns, but this sometimes leads to strange results.
Animals respond to small parts of a relevant stimulus. For example, herring gull chicks peck at the beak of the parent to get it to regurgitate – it’s a yellow beak with a red spot. A yellow pencil with a red spot on the end is enough to elicit the response. There seems to be a single key stimulus or pattern.
There is a famous anecdote from [biologist and ornithologist] Niko Tinbergen about a red postal van driving past his window. All the male sticklebacks [in his tanks] began to display toward it [because other males develop red bellies during mating season and are viewed as competition]. It’s a well-attested fact that animals seem to extract from the total gestalt just one small part of it. Tinbergen also had a picture of an oystercatcher sitting on an egg that was eight times its natural size in preference to its own egg.
What are your thoughts on the concept of pathological altruism – the idea that people might act selflessly, in the interests of others, in a way that might harm the individual?
My first book The Selfish Gene is largely about altruism. I suppose the level of altruism that humans show from the genetic point of view is pathological. We’re far more altruistic than we ought to be from a genetic point of view: giving to charity, donating blood… There is something odd about human altruism. It goes beyond what would be predicted by selfish gene theory.
We’ve talked about organisms ageing. But some organisms seem to remain “young” for ever in certain ways. Neotenisation, or juvenilisation, is the retention of juvenile features in an adult human or animal. Why does it occur?
Alister Hardy, my old professor, called it the escape from specialisation. He thought it was a major way in which evolution could advance. He thought the origin of the chordates [animals with a flexible rod supporting their dorsal or back sides, including fish, amphibians, reptiles, birds and mammals] might possibly have come from the neotenous larvae of tunicates [a marine animal that has a nerve cord, but loses it on maturing].
There is a group of tunicates – sea squirts – which look like tadpoles. All sea squirts have tadpole larvae that float around in the plankton, but these particular sea squirts have abandoned the adult stage and become sexually mature at the larval stage [thus retaining their nerve chord]. They’re called larvaceans. Hardy thought that vertebrates stem from these larval sea squirts.
Humans have bred dogs to have large eyes and shortened faces, making certain breeds look more like puppies. But you’ve described how experiments with neotenisation have taught us more than how to make pets cute.
[The evolutionary biologist] Julian Huxley was able to turn axolotls into the salamanders that they had abandoned long ago, which is wonderful. Axolotls are essentially larval salamanders. Huxley was able to encourage their metamorphosis by feeding them ground sheep thyroid, thus giving them the hormones needed to mature.
The experiment may have inspired his brother Aldous’s novel After Many a Summer [published in 1939]. The plot is about a very rich man who’s trying to prolong his life. He employs a doctor to research extending life. Eventually they work out from historical records that there’s an 18th-century aristocrat who discovered if you eat raw fish guts, you live for ever. They go to England and find the family castle of this aristocrat. Down in the dungeons, they find this great, hairy ape whistling a Mozart aria.
We are larval apes. We are juvenile apes. The conceit of the book is that this rich man can go on the fish gut diet and he’ll turn into an adult [ape]. While axolotls live much shorter lives when they are artificially induced to mature, the aristocrat in the novel ends up becoming immortal.
How have microorganisms – like viruses and bacteria – evolved alongside humans, and what do they tell us about symbiosis?
They get passed on to the next host in the gametes [the reproductive cells] of the present host. That is, if their genetic interests coincide with those of the host’s own genes. This is the case with mitochondria, which were free-living bacteria [existing outside of humans and other animals] billions of years ago. They have become incorporated into cells because they get passed down to the next host through the fertilised eggs of the mother.
A substantial number of viruses also seem to have been incorporated into the host genome, into the chromosomes – unlike mitochondria, which are bacteria and live in the cytoplasm. That’s my particular line [as first developed in The Selfish Gene]. I extrapolated it to say: not only have some viruses become incorporated into the chromosomes, but there is a sense in which you could regard all our genes as equivalent to symbiotic viruses. Although that’s probably not their origin.
Are there any areas of evolutionary research that you are following with particular interest?
The origin of life is a big mystery. I would like to understand how it happened. One of the most fashionable ideas is that life is based on RNA [ribonucleic acid] rather than DNA [deoxyribonucleic acid]. DNA is an excellent replicator, but it is not a good enzyme. Protein is a good enzyme, but can’t replicate. RNA can do both. But it’s not a great replicator and it’s not a great enzyme. It’s mediocre at both.
So you could imagine that the original replicator was RNA, because it could actually be self-catalysed. Then later on, the replication function would have been usurped by DNA and the enzyme function would have been usurped by protein.
Are there any trends in the current conception of evolution that you find concerning or misdirected?
I’m not an enthusiast for attempting to measure differential abilities in different races. It’s something you could work on but it seems to me that the motives might be suspect.
What about recent attempts to revive extinct organisms?
There are people working on woolly mammoths, for example. The DNA of frozen mammoths in Siberia is still available. Modern elephants are big enough to give birth to them, so conditions are favourable to revive them. [Colossal Biosciences in Dallas, for example, is working to bring extinct species back to life, including the woolly mammoth, using cloning and genetic engineering techniques.]
I don’t have a problem with that. Some people say things like: “We would be bringing a freak into the world. It would be unhappy.” I think if we brought enough of them into the world, they could roam the tundra, have a happy time and restore some of the lost ecology of the place.
What about instances where deeper layers of the palimpsest are being explored? Researchers at Imperial College London and Yale are analysing bird and reptile DNA to study evolution. Might we one day be able to revive the dinosaur?
You might be able to systematically chisel the way the genes are going, in order to say, well, dinosaurs looked a bit like this. They had teeth so let’s do something to bring back teeth. But you wouldn’t be bringing back a dinosaur. You would be making a dinosaur as a work of art, using a bird as a substrate.
“The Genetic Book of the Dead” is published by Apollo
This article is from New Humanist’s winter 2024 issue. Subscribe now.
