A couple of years ago, at a massive conference of neuroscientists — 35,000 attendees, scores of sessions going at any given time — I wandered into a talk that I thought would be about consciousness but proved (wrong room) to be about grasshoppers and locusts. At the front of the room, a bug-obsessed neuroscientist named Steve Rogers was describing these two creatures — one elegant, modest, and well-mannered, the other a soccer hooligan.
The grasshopper, he noted, sports long legs and wings, walks low and slow, and dines discreetly in solitude. The locust scurries hurriedly and hoggishly on short, crooked legs and joins hungrily with others to form swarms that darken the sky and descend to chew the farmer’s fields bare.
Related, yes, just as grasshoppers and crickets are. But even someone as insect-ignorant as I could see that the hopper and the locust were wildly different animals — different species, doubtless, possibly different genera. So I was quite amazed when Rogers told us that grasshopper and locust are in fact the same species, even the same animal, and that, as Jekyll is Hyde, one can morph into the other at alarmingly short notice.
Not all grasshopper species, he explained (there are some 11,000), possess this morphing power; some always remain grasshoppers. But every locust was, and technically still is, a grasshopper — not a different species or subspecies, but a sort of hopper gone mad. If faced with clues that food might be scarce, such as hunger or crowding, certain grasshopper species can transform within days or even hours from their solitudinous hopper states to become part of a maniacally social locust scourge. They can also return quickly to their original form.
In the most infamous species, Schistocerca gregaria, the desert locust of Africa, the Middle East and Asia, these phase changes (as this morphing process is called) occur when crowding spurs a temporary spike in serotonin levels, which causes changes in gene expression so widespread and powerful they alter not just the hopper’s behaviour but its appearance and form. Legs and wings shrink. Subtle camo colouring turns conspicuously garish. The brain grows to manage the animal’s newly complicated social world, which includes the fact that, if a locust moves too slowly amid its million cousins, the cousins directly behind might eat it.
How does this happen? Does something happen to their genes? Yes, but — and here was the point of Rogers’s talk — their genes don’t actually change. That is, they don’t mutate or in any way alter the genetic sequence or DNA. Nothing gets rewritten. Instead, this bug’s DNA — the genetic book with millions of letters that form the instructions for building and operating a grasshopper — gets reread so that the very same book becomes the instructions for operating a locust. Even as one animal becomes the other, as Jekyll becomes Hyde, its genome stays unchanged. Same genome, same individual, but, I think we can all agree, quite a different beast.
Transforming the hopper is gene expression — a change in how the hopper’s genes are ‘expressed’, or read out. Gene expression is what makes a gene meaningful, and it’s vital for distinguishing one species from another. We humans, for instance, share more than half our genomes with flatworms; about 60 per cent with fruit flies and chickens; 80 per cent with cows; and 99 per cent with chimps. Those genetic distinctions aren’t enough to create all our differences from those animals — what biologists call our particular phenotype, which is essentially the recognisable thing a genotype builds. This means that we are human, rather than wormlike, flylike, chickenlike, feline, bovine, or excessively simian, less because we carry different genes from those other species than because our cells read differently our remarkably similar genomes as we develop from zygote to adult. The writing varies — but hardly as much as the reading.
This raises a question: if merely reading a genome differently can change organisms so wildly, why bother rewriting the genome to evolve? How vital, really, are actual changes in the genetic code? Do we even need DNA changes to adapt to new environments? Is the importance of the gene as the driver of evolution being overplayed?
You’ve probably noticed that these questions are not gracing the cover of Time or haunting Oprah, Letterman, or even TED talks. Yet for more than two decades they have been stirring a heated argument among geneticists and evolutionary theorists. As evidence of the power of rapid gene expression mounts, these questions might (or might not, for pesky reasons we’ll get to) begin to change not only mainstream evolutionary theory but our more everyday understanding of evolution.
Twenty years ago, phase changes such as those that turn grasshopper to locust were relatively unknown, and, outside of botany anyway, rarely viewed as changes in gene expression. Now, notes Mary Jane West-Eberhard, a wasp researcher at the Smithsonian Tropical Research Institute in Costa Rica, sharp phenotype changes due to gene expression are ‘everywhere’. They show up in gene-expression studies of plants, microbes, fish, wasps, bees, birds, and even people. The genome is continually surprising biologists with how fast and fluidly it can change gene expression — and thus phenotype.
These discoveries closely follow the recognition, during the 1980s, that gene-expression changes during very early development — such as in embryos or sprouting plant seeds — help to create differences between species. At around the same time, genome sequencing began to reveal the startling overlaps mentioned above between the genomes of wildly different creatures. (To repeat: you are 80 per cent cow.)
Shapeshifter: the locust. Photo by Ocean/Corbis
Gregory Wray, a biologist at Duke University in North Carolina who studies fruit flies, sees this flexibility of genomic interpretation as a short path to adaptive flexibility. When one game plan written in the book can’t provide enough flexibility, fast changes in gene expression — a change in the book’s reading — can provide another plan that better matches the prevailing environment.
‘Different groups of animals succeed for different reasons,’ says Wray. ‘Primates, including humans, have succeeded because they’re especially flexible. You could even say flexibility is the essence of being a primate.’
According to Wray, West-Eberhard and many others, this recognition of gene expression’s power requires that we rethink how we view genes and evolution. For a century, the primary account of evolution has emphasised the gene’s role as architect: a gene creates a trait that either proves advantageous or not, and is thus selected for, changing a species for the better, or not. Thus, a genetic blueprint creates traits and drives evolution.
This gene-centric view, as it is known, is the one you learnt in high school. It’s the one you hear or read of in almost every popular account of how genes create traits and drive evolution. It comes from Gregor Mendel and the work he did with peas in the 1860s. Since then, and especially over the past 50 years, this notion has assumed the weight, solidity, and rootedness of an immovable object.
But a number of biologists argue that we need to replace this gene-centric view with one that more heavily emphasises the role of gene expression — that we need to see the gene less as an architect and more as a member of a collaborative remodelling and maintenance crew.
‘We have a more complicated understanding of football than we do genetics and evolution. Nobody thinks just the quarterback wins the game’
They ask for something like the rejection a century ago of the Victorian-era ‘Great Man’ model of history. This revolt among historians recast leaders not as masters of history, as Tolstoy put it, but as servants. Thus the Russian Revolution exploded not because Marx and Lenin were so clever, but because fed-up peasants created an impatience and an agenda that Marx articulated and Lenin ultimately hijacked. Likewise, D-Day succeeded not because Eisenhower was brilliant but because US and British soldiers repeatedly improvised their way out of disastrously fluid situations. Wray, West-Eberhard and company want to depose genes likewise. They want to cast genes not as the instigators of change, but as agents that institutionalise change rising from more dispersed and fluid forces.
This matters like hell to people like West-Eberhard and Wray. Need it concern the rest of us?
It should. We are rapidly entering a genomic age. A couple of years ago, for instance, I became one of what is now almost a half-million 23andMe customers, paying the genetic-profiling company to identify hundreds of genetic variants that I carry. I now know ‘genes of interest’ that reveal my ancestry and help determine my health. Do I know how to make sense of them? Do they even make sense? Sometimes; sometimes not. They tell me, for instance, that I’m slightly more likely than most to develop Alzheimer’s disease, which allows me to manage my health accordingly. But those genes also tell me I should expect to be short and bald, when in fact I’m 6’3” with a good head of hair.
Soon, it will be practical to buy my entire genome. Will it tell me more? Will it make sense? Millions of people will face this puzzle. Along with our doctors, we’ll draw on this information to decide everything from what drugs to take to whether to have kids, including kids a few days past conception — a true make-or-break decision.
Yet we enter this genomic age with a view of genetics that, were we to apply it, say, to basketball, would reduce that complicated team sport to a game of one-on-one. A view like that can be worse than no view. It tempts you to think you understand the game when you don’t. We need something more complex.
‘And it’s not as if people can’t handle things more complex,’ says Wray. ‘Educated people handle ideas more complex than this all the time. We have a more complicated understanding of football than we do genetics and evolution. Nobody thinks just the quarterback wins the game.
‘We’re stuck in an outmoded way of thinking that should have fallen long ago.’
This outmoded thinking grew from seeds planted 150 years ago by Gregor Mendel, the monk who studied peas. Mendel spent seven years breeding peas in a five-acre monastery garden in the town of Brno, now part of the Czech Republic. He crossed plants bearing wrinkled peas with those bearing smooth peas, producing 29,000 plants altogether. When he was done and he had run the numbers, he had exposed the gene.
This was the Holy Shit! moment that launched genetics’ Holy Shit! century
Mendel didn’t expose the physical gene, of course (that would come a century later), but the conceptual gene. And this conceptual gene, revealed in the tables and calculations of this math-friendly monk, seemed an agent of mathematical neatness. Mendel’s thousands of crossings showed that the traits he studied — smooth skin versus wrinkled, for instance, or purple flower versus white — appeared or disappeared in consistent ratios dictated by clear mathematical formulas. Inheritance appeared to work like algebra. Anything so math-friendly had to be driven by discrete integers.
It was beautiful work. Yet when Mendel first published his findings in 1866, just seven years after Charles Darwin’s On the Origin of Species, no one noticed. Starting in 1900, however, biologists rediscovering his work began to see that these units of heredity he’d discovered — dubbed genes in 1909 — filled a crucial gap in Darwin’s theory of evolution. This recognition was the Holy Shit! moment that launched genetics’ Holy Shit! century. It seemed to explain everything. And it saved Darwin.
Darwin had legitimised evolution by proposing for it a viable mechanism — natural selection, in which organisms with the most favourable traits survive and multiply at higher rates than do others. But he could not explain what created or altered traits.
Mendel could. Genes created traits, and both would spread through a population if a gene created a trait that survived selection.
That much was clear by 1935. Naturally, some kinks remained, but more math-friendly biologists soon straightened those out. This took most of the middle part of the 20th century. Biologists now call this decades-long project the modern evolutionary synthesis. And it was all about maths.
The most vital calculations were run in the 1930s, when Ronald Fisher, J B S Haldane and Sewall Wright, two brilliant Brits and an American working more or less separately, worked out two key problems. The first was how Mendel’s rather binary genetic model could create not just binary differences such as smooth versus wrinkled peas but the gradual evolutionary change of the sort that Darwin described. Fisher, Haldane and Wright, working the complicated maths of how multiple genes interacted through time in a large population, showed that significant evolutionary change revealed itself as many small changes yielded a large effect, just as a series of small nested equations within a long algebra equation could.
The second kink was tougher. If organisms prospered by out-competing others, why did humans and some other animals help one another? This might seem a non-mathy problem. Yet Fisher, Haldane and Wright solved it too with maths, devising formulas quantifying precisely how altruism could be selected for. Some animals act generously, they explained, because doing so can aid others, such as their children, parents, siblings, cousins, grandchildren, or tribal mates, who share or might share some of their genes. The closer the kin, the kinder the behaviour. Thus, as Haldane once said, ‘I would lay down my life for two brothers or eight cousins.’
Thus maths reconciled Mendel and Darwin and made modern genetics and evolutionary theory a coherent whole. Watson and Crick’s 1953 discovery of the structure of DNA simply iced the cake: now we knew the structure that performed the maths.
Finally, in the early 1960s, yet another Brit named William Hamilton (a funny statistician with a shaggy haircut) and an American named George Williams (kind and whipsmart, with an abominable haircut and beard) upped the ante on the gene’s primacy: with fancy maths, they argued that we should view any organism, including any human, as merely a sort of courier for genes and their traits. This flipped the usual thinking. It made the gene vital and the organism expendable. Our genes did not exist for us. We existed for them. We served only to carry these chemical codes forward through time, like those messengers in old sword-and-sandal war movies who run non-stop for days to deliver data and then drop dead. A radical idea. Yet it merely extended the logic of kin selection, in which any gene-courier — say, a mom watching her children’s canoe overturn — would risk her life to let her kin carry forth her DNA.
This notion of the gene as the unit selected, and the organism as a kludged-up cart for carrying it through time, placed the gene smack at the centre of things. It granted the gene something like agency.
At first, not even many academics paid this any heed. This might be partly because people resist seeing themselves as donkey carts. Another reason was that neither Hamilton nor Williams were masterly communicators.
But 15 years after Hamilton and Williams kited this idea, it was embraced and polished into gleaming form by one of the best communicators science has ever produced: the biologist Richard Dawkins. In his magnificent book The Selfish Gene (1976), Dawkins gathered all the threads of the modern synthesis — Mendel, Fisher, Haldane, Wright, Watson, Crick, Hamilton, and Williams — into a single shimmering magic carpet.
These days, Dawkins makes the news so often for buffoonery that some might wonder how he ever became so celebrated. The Selfish Gene is how. To read this book is to be amazed, entertained, transported. For instance, when Dawkins describes how life might have begun — how a randomly generated strand of chemicals pulled from the ether could happen to become a ‘replicator’, a little machine that starts to build other strands like itself, and then generates organisms to carry it — he creates one of the most thrilling stretches of explanatory writing ever penned. It’s breathtaking.
Dawkins reveals the gene as not just the centre of the cell but the centre of all life, agency, and behaviour
Dawkins assembles genetics’ dry materials and abstract maths into a rich but orderly landscape through which he guides you with grace, charm, urbanity, and humour. He replicates in prose the process he describes. He gives agency to chemical chains, logic to confounding behaviour. He takes an impossibly complex idea and makes it almost impossible to misunderstand. He reveals the gene as not just the centre of the cell but the centre of all life, agency, and behaviour. By the time you’ve finished his book, or well before that, Dawkins has made of the tiny gene — this replicator, this strip of chemicals little more than an abstraction — a huge, relentlessly turning gearwheel of steel, its teeth driving smaller cogs to make all of life happen. It’s a gorgeous argument. Along with its beauty and other advantageous traits, it is amenable to maths and, at its core, wonderfully simple.
Unfortunately, say Wray, West-Eberhard and others, it’s wrong.
Wray and West-Eberhard don’t say that Dawkins is dead wrong. They and other evolutionary theorists — such as Massimo Pigliucci, professor of philosophy at the City University of New York; Eva Jablonka, professor of mathematics education at King’s College, London; Stuart Kauffman, professor of biochemistry and mathematics at the University of Vermont; Stuart A Newman, professor of cell biology and anatomy at the New York Medical College; and the late Stephen Jay Gould, to name a few — have been calling for an ‘extended modern synthesis’ for more than two decades. They do so even though they agree with most of what Dawkins says a gene does. They agree, in essence, that the gene is a big cog, but would argue that the biggest cog doesn’t necessarily always drive the other cogs. In many cases, they drive it. The gene, in short, just happens to be the biggest, most obvious part of the trait-making inheritance and evolutionary machine. But not the driver.
Another way to put it: Mendel stumbled over the wrong chunk of gold.
Mendel ran experiments that happened to reveal strong single-gene dynamics whose effects — flower colour, skin texture — can seem far more significant than they really are. Many plant experiments since then, for instance, have shown that environmental factors such as temperature changes can spur gene-expression changes that alter a plant far more than Mendel’s gene variants do. As with grasshoppers, a new environment can quickly turn a plant into something almost unrecognisable from its original form. If Mendel had owned a DNA microarray machine and was in the habit of tracking gene expression changes, he might have spotted these. But microarray machines didn’t exist, so he crossed plants instead, and saw just one particularly obvious way that an organism can change.
The gene-centric view is thus ‘an artefact of history’, says Michael Eisen, an evolutionary biologist who researches fruit flies at the University of California, Berkeley. ‘It rose simply because it was easier to identify individual genes as something that shaped evolution. But that’s about opportunity and convenience rather than accuracy. People confuse the fact that we can more easily study it with the idea that it’s more important.’
The gene’s power to create traits, says Eisen, is just one of many evolutionary mechanisms. ‘Evolution is not even that simple. Anyone who’s worked on systems sees that natural selection takes advantage of the most bizarre aspects of biology. When something has so many parts, evolution will act on all of them.
‘It’s not that genes don’t sometimes drive evolutionary change. It’s that this mutational model — a gene changes, therefore the organism changes — is just one way to get the job done. Other ways may actually do more.’
Like what other ways?
There are several, but one called genetic accommodation is, according to West-Eberhard, particularly powerful and overlooked.
Individual bees morph from worker to guard to scout by gene expression alone, depending on the needs of the hive
In the social wasps that West-Eberhard has been studying in Costa Rica since 1979, many of the most important distinctions among a colony’s individuals rise not from differences in their genomes, which vary little, but from the plasticity born of gene expression. This starts with the queen, who is genetically identical to her thousands of sisters yet whose gene expression makes her not only larger, but singles her out as the colony’s reproductive unit. Likewise with most honeybees. In social honeybees, the differences between workers, guards, and scouts all arise from gene expression, not gene sequence. Individual bees morph from one form to another — worker to guard to scout — by gene expression alone, depending on the needs of the hive.
Like Wray, Pigliucci and others, West-Eberhard has long tried to rescue the centrality of gene expression from the ‘cyclic amnesia’ that she says has ignored 150 years of evidence that gene selection’s role in evolution is overplayed. West-Eberhard is a particularly articulate advocate. Yet she’s frustrated at how little she’s been able to change things.
As a David to Dawkins’s Goliath, West-Eberhard faces distinct challenges. For starters, she’s a she while Dawkins is a he, which should not matter but does. And while Dawkins holds forth from Oxford, one of the most prestigious universities on earth, and deploys from London an entire foundation in his name, West-Eberhard studies and writes from a remote outpost in Central America. Dawkins commands locust-sized audiences any time he speaks and probably turns down enough speaking engagements to fill five calendars; West-Eberhard speaks mainly to insect-crazed colleagues at small conferences. Dawkins wrote a delicious 300-page book that has sold tens of millions of copies; West-Eberhard has written a bunch of fine obscure papers and an 800-page tome, Developmental Plasticity and Evolution (2003), which, though not without its sweet parts, is generally consumed as a meal of obligation.
She does have her pithy moments. ‘The gene does not lead,’ she says. ‘It follows.’
There lies the quick beating heart of her argument: the gene follows. And one of the ways the gene follows is through this process called genetic accommodation. Genetic accommodation is a clunky term for a graceful process. It takes a moment to explain. But bear with me a moment, and you’ll understand how you, dear reader, could evolve into a fast and deadly predator.
Genetic accommodation involves a three-step process.
First, an organism (or a bunch of organisms, a population) changes its functional form — its phenotype — by making broad changes in gene expression. Second, a gene emerges that happens to help lock in that change in phenotype. Third, the gene spreads through the population.
For example, suppose you’re a predator. You live with others of your ilk in dense forest. Your kind hunts by stealth: you hide among trees, then jump out and snag your meat. You needn’t be fast, just quick and sneaky.
Then a big event — maybe a forest fire, or a plague that kills all your normal prey — forces you into a new environment. This new place is more open, which nixes your jump-and-grab tactic, but it contains plump, juicy animals, the slowest of which you can outrun if you sprint hard. You start running down these critters. As you do, certain genes ramp up expression to build more muscle and fire the muscles more quickly. You get faster. You’re becoming a different animal. You mate with another fast hunter, and your kids, hunting with you from early on, soon run faster than you ever did. Via gene expression, they develop leaner torsos and more muscular, powerful legs. By the time your grandchildren show up, they seem almost like different animals: stronger legs, leaner torsos, and they run way faster than you ever did. And all this has happened without taking on any new genes.
Then a mutation occurs in one grandkid. This mutation happens to create stronger, faster muscle fibres. This grandchild of yours can naturally and easily run faster than her fastest siblings and cousins. She flies. Her children inherit the gene, and because their speed wows their mating prospects, they mate early and often, and bear lots of kids. Through the generations, this sprinter’s gene thus spreads through the population.
Now the thing is complete. Your descendants have a new gene that helps secure the adaptive trait you originally developed through gene expression alone. But the new gene didn’t create the new trait. It just made it easier to keep a trait that a change in the environment made valuable. The gene didn’t drive the train; it merely hopped aboard. Had the gene showed up earlier (either through mutation or mating with an outsider), back when you lived in the forest and speed didn’t mean anything, it would have given no advantage. Instead of being selected for and spreading, the gene would have disappeared or remained in just a few animals. But because the gene was now of value, the population took it in, accommodated it, and spread it wide.
This isn’t the gene-centric world in which genotype creates phenotype. It’s a phenotype accommodating a new genotype by making it relevant.
Gene Robinson, an entomologist who studies honeybees at the University of Illinois, says genetic accommodation probably helped to create African honeybees, the ‘killer bee’ subspecies that is genetically distinct from the sweeter European honeybees that most beekeepers keep. Honeybee hives in certain parts of Africa, he says, were and are raided by predators more often than hives elsewhere, so their inhabitants had to react more sharply to attacks. This encouraged gene-expression changes that made the African bees respond more aggressively to threat. When new genes showed up that reinforced this aggression, those genes would have been selected for and spread through the population. This, Robinson says, is quite likely how African bees became genetically distinct from their European honeybee cousins. And they’d have been led there not by a gene, but by gene expression.
After several weeks of reading and talking to this phenotypic plasticity crowd, I phoned Richard Dawkins to see what he thought of all this. Did genes follow rather than lead? I asked him specifically about whether processes such as gene accommodation might lead instead. Then he did something so slick and wonderful I didn’t quite realise what he’d done till after we hung up: he dismissed genetic accommodation… by accommodating it. Specifically, he said that genetic accommodation doesn’t really change anything, because since the gene ends up locking in the change and carrying it forward, it all comes back to the gene anyway.
‘This doesn’t modify the gene-centric model at all,’ he said. ‘The gene-centric model is all about the gene being the unit in the hierarchy of life that is selected. That remains the gene.’
‘He’s backfilling,’ said West-Eberhard. ‘He and others have long been arguing for the primacy of an individual gene that creates a trait that either survives or doesn’t.’
Yet West-Eberhard understands why many biologists stick to the gene-centric model. ‘It makes it easier to explain evolution,’ she says. ‘I’ve seen people who work in gene expression who understand all of this. But when they get asked about evolution, they go straight to Mendel. Because people understand it more easily.’ It’s easy to see why: even though life is a zillion bits of biology repeatedly rearranging themselves in a webwork of constantly modulated feedback loops, the selfish-gene model offers a step-by-step account as neat as a three-step flow chart. Gene, trait, phenotype, done.
In other words, the gene-centric model survives because simplicity is a hugely advantageous trait for an idea to possess. People will select a simple idea over a complex idea almost every time. This holds especially in a hostile environment, like, say, a sceptical crowd. For example, Sean B Carroll, professor of molecular biology and genetics at the University of Wisconsin, spends much of his time studying gene expression, but usually uses gene-centric explanations, because when talking to the public, he finds a simple story is a damned good thing to have.
Which drives West-Eberhard nuts.
‘Dawkins understands very well that gene expression is powerful,’ she says. ‘He sees things are more complex than a selfish gene. He could turn on its head the whole language.’
Yet Dawkins, and with him much of pop science, sticks to the selfish gene. The gene explains all. So far it has worked. The extended synthesis crowd has published scores of papers, quite a few books, and held meetings galore. They have changed the way many biologists think about evolution, at least when those biologists are thinking. But they have scarcely touched the public’s understanding. And they have not found a way to displace a meme so powerful as the selfish gene.
This meme, methinks, forms the true bone of contention and the true obstacle to progress. It’s one of the gruesome beauties of this whole mess that Dawkins himself coined the term meme, and did so in The Selfish Gene. He defined it as a big idea that competes for dominance in a tough environment — an idea that, like a catchy tune or a good joke, ‘propagates itself by leaping from brain to brain’. The selfish-gene meme has done just that. It has made of evolutionary theory a vehicle for its replication. The selfish gene has become a selfish meme.
If you’re West-Eberhard or of like mind, what are you to replace it with? The slave-ish gene? Not likely to leap from brain to brain. The accommodating gene? Mmmmmaybe — but I’m betting that phrase lacks the needed bling. And as West-Eberhard notes, either phrase still encourages a focus on single genes. And ‘evolution is not about single genes,’ she says. ‘It’s about genes working together.’
Better then to speak not of genes but the genome — all your genes together. And not the genome as a unitary actor, but the genome in conversation with itself, with other genomes, and with the outside environment. If you’re into gene expression — if grasshoppers and honeybees and genetic accommodation are to be believed — it’s those conversations that define the organism and drive the evolution of new traits and species. It’s not a selfish gene or a solitary genome. It’s a social genome.
What would Mendel think of that? Let’s play this out.
Mendel actually studied bees as a boy, and he studied them again for a couple years after he finished his pea-plant studies. In crossbreeding two species at the monastery, he accidentally created a strain of bees so vicious that he couldn’t work with them. If he’d had a microarray machine, he, like Gene Robinson, could have studied how much of the bees’ aggression rose from changes in the genetic code or how much rose from changes in gene expression. If he had, the father of genetics might have seen right then that traits change and species evolve not just when genes change, but when gene expression does. He might have discovered not just genes, but genetic accommodation. Not the selfish gene, but the social genome.
Alas, no such equipment existed, and Mendel worked in a monastery in the middle of town. His vicious bees promised not a research opportunity but trouble. So he killed them. He would found genetics not through a complex story of morphing bees, but through a simple tale of one pea wrinkled, one pea smooth.
Correction, 3 December 2013: the original version of this article stated that Sewall Wright was a Brit. He was in fact an American.