She Has Her Mother's Laugh: The Powers, Perversions, and Potential of Heredity (63 page)

Whenever this sort of inequality emerged in a Nootka village, it could endure for a few centuries before it collapsed. Droughts and other disasters could wipe out the advantages that some families had over others. It's likely that inequality was just as fragile in all hunter-gatherer societies across the world. But the rise of agriculture allowed inequality to explode and endure. In the Near East, for example, foragers gathered wild plants together and stored them in communal granaries. As they switched to farming, they claimed rights to land for growing crops and built private granaries to store their harvests. Farmers who planted superior crops ended up with extra food that they could barter for goods. They could then pass down their land and those goods to their children, who could start farming with huge advantages.

It's obvious that inheriting PKU from one's parents is not the same as inheriting the knowledge of how to make nardoo bread. The first inheritance involves the copying of genetic information that gets brought together in an embryo. The second comes about through years of teaching, expressed in actions and language. Yet they are not utterly different either. Both kinds of inheritance are part of the variation from person to person and from population to population. And both can sustain that variation across generations.

At the dawn of the twentieth century, scientists came to limit the word
heredity
to genes. Before long, this narrow definition spread its influence far beyond genetic laboratories. It hangs like a cloud over our most personal experiences of heredity, even if we can't stop trying to smuggle the old traditions of heredity into the new language of genes.

We call genetic disorders family curses. A family of rich real estate barons rationalizes its wealth with mysterious genes for success. Genealogy began as an ancient practice of legitimization through ancestry, but we still depend on it to explain how we came to be. When birth certificates and immigration records fail us, we take up DNA to draw branches further back and farther out. We exult in discovering a link to some famous figure in history, as if carrying their alleles makes us special—ignoring the fact that beyond a few generations, we share little or no DNA with our ancestors. We take DNA tests to find out if we're full-blooded Irish or Cherokee or Egyptian, using sixteenth-century terms that started out as ways to describe racehorses or to divide humans into arbitrary categories—despite the fact that the evidence from that DNA chews holes in those barriers like a termite invasion. There is certainly a history to each chunk of our genetic material, but each one hurtles back through human history in a different direction, leaping from continent to continent. A human genome is a shredded, shuffled sampling of DNA, both from humans and from our extinct near-human relatives.

We think of heredity as limited to what normally happens in human families. Two parents combine half their DNA to produce a new offspring, their genes obeying Mendel's Law. In truth, heredity does not stop at conception's door. Cells continue to divide, and their daughter cells inherit everything inside them—their mitochondria, their proteins, their chromosomes, and the epigenetic network that gives each cell its state. Our bodies are walking genealogies, the branches distinguished by locked-in networks of genes, mosaic mutations—even by chimeric origins in different people. Germ cells can extend this heredity into new lives, but August Weismann's barrier is far from absolute. An untold number of animals have gained a cancerous immortality by sending forth their tumors to burrow into new hosts for thousands of years on land and at sea.

None of this is to say that Weismann himself was wrong. He gave science a new way to think about heredity, one that prepared the ground for the recognition of Mendel's discoveries. By the early 1900s, Mendel's Law was allowing geneticists to begin making sense of human heredity, explaining the now-you-see-it, now-you-don't evasion of traits through the generations that left even Darwin baffled. The easiest mysteries it solved were diseases caused by a single dominant allele or a pair of recessive ones like PKU. But for other traits—including ones as seemingly simple as height—heredity has become an ocean of explanation. The effect that our biological past has on our height has been shattered into thousands of pieces of influence.

Mendel's Law also turned out to be exquisitely fragile. It is regularly broken. Gene drives regularly get the better of Mendel's Law, carrying genes throughout populations, even at risk of pushing species to extinction. Many species of animals, plants, and fungi themselves sometimes obey Mendel's Law and sometimes find a different way to pass genes down to future generations. Some become both father and mother. They use their own sperm to fertilize their own eggs. Or they simply recombine the chromosomes within a single cell, which then develops into an offspring. Others dispense with gametes altogether, cloning themselves. These species are not rare flukes; they live around us. They grow into forests and coral reefs. They make our bread and beer.

Our anthropocentrism also makes it easy to forget that Mendel's Law is young. The universe was born with the speed of light fixed at 186,000 miles a second. The mass of an electron was set. And Mendel's Law was nowhere in the cosmos to be found. It evolved much later, as far as we know on only one planet. But on that water-coated rock, heredity had already been unspooling for billions of years when Mendel's Law evolved. The microbes and viruses that until then were the sole residents of Earth for over half the history of life did not reproduce by combining germ cells. Nor do they do so today. They follow rules of their own. They can make near-identical copies of their DNA. But that DNA can also slip from one microbe to another, producing patchworks that might never have evolved if heredity could only travel vertically. Microbes evolved new kinds of heredity of their own. It
was only in the early 2000s that scientists discovered that many species used CRISPR to gain a defense against viruses—a defense that their descendants could then inherit.

We cannot understand the natural world with a simplistic notion of genetic heredity. And some scientists have likewise argued that we must expand our definition of
heredity
again, to take into account other channels as well—be they culture, epigenetic marks, hitchhiking microbes, or channels we don't even know about yet. In the 1980s, Marcus Feldman and a number of other researchers began trying to build a theory of heredity that could include both culture and genes. Since then, others have tried to widen the theory even more. Russell Bonduriansky of the University of New South Wales in Australia and Troy Day of Queen's University in Ontario, Canada, believe it's time to build mathematical equations that can unite genetic and nongenetic forms of heredity in a single description. They lay out their vision in a 2018 book,
Not Only Genes.

Bonduriansky and Day argue that the previous century of research on heredity was based on a fallacy. Geneticists didn't simply champion the gene by finding evidence for it. They rejected the possibility that anything other than genes could carry heredity. Yet the existence of one channel did not necessarily rule out the other. “This purely genetic concept of heredity was never firmly backed by evidence or logic,” Bonduriansky and Day declare.

As the genetic concept took hold, research into nongenetic forms faded away. The field's reputation was stained by scandals, as some experiments that supposedly supported nongenetic heredity proved to be shoddy or even fraudulent. But even careful scientists were at a disadvantage. The effects of genes can have a downright arithmetic precision. Simply breeding peas or flies reveals profound facts about how genes are inherited. Nongenetic forms of heredity are harder to distinguish from influences of the environment, and they can be more prone to vanish. Researchers who have tried to document nongenetic heredity have thus had to play a long game of catch-up. Linnaeus laid his eyes on the monstrous
Peloria
in the 1740s. When I visited Robert Martienssen 170 years later, he was still struggling to discover what keeps them monstrous after all these generations.

The debate over heredity had reached a different stage. Both sides accepted the reality of the other. No champion of nongenetic heredity denies the power of genes. And of the geneticists I've spoken to, none has outright rejected the idea that heredity can be sustained by things other than genes. The fight now is over importance. Some geneticists don't see much to be gained by investigating nongenetic heredity. Other biologists believe that the only way to make sense of traits they find in organisms is to understand how they're transmitted—and sometimes that search will take them beyond genes.

One argument in favor of genes—and against nongenetic heredity—is that genes have sticking power. Our cells are packed with dedicated swarms of proteins and RNA molecules that work together to copy genes, ensuring that new copies are virtually identical to the original ones. The low rate of mutations in our DNA allows an allele to endure for generations. Its sticking power gives natural selection enough time to favor it over other alleles, and to drive evolutionary change.

Nongenetic heredity can be far more fleeting. Water fleas, tiny invertebrates that live in ponds and streams, use a form of nongenetic heredity to escape predators. If they pick up the odor of a predatory fish, they grow spikes on their heads and tails, making it more likely that a fish will spit them out rather than swallow them. Female water fleas will then produce offspring that grow spikes early in development, even in the absence of any odor of a predator. This shift will endure for several generations—but then it fades away. A new generation of water fleas emerges spike-free. This sort of heredity can't drive evolutionary change, because natural selection can't favor spiked water fleas over spikeless ones for very long.

Yet Bonduriansky and Day reject this argument against the importance of nongenetic heredity. In some cases, it can actually be quite durable. The fact that Linnaeus's monstrous toadflax are still monstrous demonstrates that heredity can flow down an epigenetic channel for centuries—at least in toadflax. If we accept culture as a form of heredity, then we can trace some cultural traditions for tens of thousands of years. And even when nongenetic heredity is fleeting, it can still have a big influence on a species. By
programming their descendants with spikes and other protections, animals and plants can enjoy long-term evolutionary success even as their environment changes. This success can have effects that ripple outward across an entire food web. A water flea's spikes allow it to increase in numbers while keeping its predators hungry.

Nongenetic heredity matters for another reason: It can potentially steer evolution. Under some conditions, for example, natural selection may favor tall plants over short ones. Plants can reach great heights if they inherit the right alleles, but nongenetic factors can also influence how tall a plant gets. If nongenetic factors make tall plants even taller, they will be able to have even more offspring. In other cases, nongenetic heredity may work against genes, bringing evolution to a standstill.

In
Not Only Genes
, Bonduriansky and Day remain agnostic about just how important nongenetic heredity will turn out to be. They are not drumming up hype about epigenetic memories of past lives. They simply consider the question both important and unanswered. Bonduriansky and Day have developed mathematical equations and conceptual tools they hope will make it possible to study both forms of heredity at the same time, in the same organisms. They argue that a combination of both kinds of heredity could help address some of the biggest questions scientists still have about the history of life—why we get old, for example, how peacock tails and other extravagant courtship displays evolve, how new species arise. Even human history could benefit from an expanded view of heredity.

If you've recently enjoyed a cone of ice cream or a slice of Brie, for instance, you are experiencing one of the more bizarre results of the Agricultural Revolution. As a rule, mammals don't consume milk in any form once they stop nursing. After weaning, they stop producing lactase, the enzyme required to break down lactose sugar. The same is true for about two-thirds of people worldwide. For them, consuming milk can be an uncomfortable experience, leading to symptoms including bloating and diarrhea. But the remaining two billion or so people can continue to drink milk and eat dairy foods as adults. They have inherited mutations that lead them to persist in making lactase.

Scientists have found a number of these mutations in the same region of the genome. They alter a genetic switch that controls LCT, the gene for lactase, keeping it from shutting down after weaning. The mutations show signs of having been favored by natural selection within the past few thousand years. And they are found in people who can trace their ancestry back to places with a deep history of cattle herding, such as East Africa, the Near East, and northwestern Europe.

All this evidence aligns nicely. It suggests that after some people domesticated cattle, a mutation became common that allowed them to consume milk. At this point, it's tempting to declare the case closed. But Bonduriansky and Day point out a paradox embedded in this story. Before the domestication of cattle, very few people inherited LCT mutations. The early cattle herders, in other words, were mostly lactose intolerant. It's hard to see how they would have taken up the practice of consuming milk if it made most of them sick to their stomachs. And if they didn't, then there would be no opportunity for the lactose-tolerant people to thrive on milk and spread their alleles.

The way out of this paradox is to recognize that two kinds of heredity were playing out at the same time among early herders: the genetic heredity of LCT mutations, and the cultural heredity of milk-consuming traditions. The cultural practice of herding cattle, sheep, and goats started out mainly as a way to get meat. But later the herders used their creativity to discover other kinds of foods that their animals could provide. They began milking their animals. At first, the lactose-intolerant herders may have only drunk a little milk. But as the milk soured, they may also have discovered that it was easier to digest milk by first turning it into yogurt and cheese—two foods that have much less lactose than regular milk. In Poland, researchers have discovered a 7,200-year-old sieve with milk fat still embedded in it—
a sign of early cheese-making.