WHEN THE DARK of moonless nights arrives, the one-fin flashlight fish emerges from its hiding place.
This fish (scientifically known as Photoblepharon palpebratus) lives in the waters off the Banda Islands, a scattered archipelago in Indonesia. It spends the daylight hours resting in caves a hundred feet or more underwater. When the sea turns black, the fish swims out of its caves, up to the surface waters. As it hunts for little invertebrates, its body emits a cream-colored light.
Like any animal, the flashlight fish is actually a collection of organs. Its skin acts as a barrier, protecting it from the surrounding sea. Its gills draw oxygen. Its stomach digests its prey. Each organ is distinct, because its cells produce a distinctive collection of molecules and operate a distinctive network of genes. The light made by the fish comes from a pair of jelly-bean–shaped structures under each eye. To produce their light, the cells in those jelly beans manufacture proteins that glow.
Shining a light might not seem a very smart thing to do when you’re a small fish swimming in a sea of predators. But flashlight fish can actually use it to escape their enemies. To flee, they dash straight ahead for a while, their light organs tracing a forward-moving line. They then roll each light organ into a pocket in their head. The fish suddenly go dark and then break away from their straight line, leaving predators barreling forward into empty water.
Their light organs thus help the fish survive long enough to reproduce. The males cast sperm into the water to fertilize female eggs, which develop into larvae and finally into mature fish. Like engenders like is as true for flashlight fish as for any other animal. Every new generation developed fins like their ancestors did, along with eyes, jaws, and gills. And light organs.
In 1971, a pair of scientists—Yata Haneda of the Yokosuka City Museum and Frederick Tsuji of the University of Pittsburgh—journeyed to the Banda Islands to investigate the one-fin flashlight fish. In the evenings, they would push off from shore in a canoe. Eventually they would extinguish their lights and gaze into the water, searching for the fish’s gleam. When Haneda and Tsuji caught some in a net, they put the animals in jars of seawater and later dissected the light organs. Even after they were carved out of the animals, the organs still glowed. (Banda fishermen use the light organ as a lure, putting it on a hook, where it can glow for hours.)
Haneda and Tsuji inspected the light organ cells under a microscope to understand how they worked. It was possible that the fish produced their light like fireflies. Fireflies carry a gene in their DNA for a protein called luciferin. The insects store luciferin in the cells in their tail. When they want to send a signal to their fellow fireflies, they use other proteins to alter the luciferin, unleashing its stored light. Fireflies inherit the luciferin gene from their parents, along with the rest of their genes.
But the one-fin flashlight fish has no genes for making light, Haneda and Tsuji discovered. The glowing cells in their light organ do not belong to the fish itself. They are bacteria.
They are not just any bacteria, however. If you look in the light organs of any one-fin flashlight fish, the glowing microbes always belong to the same strain, known as Candidatus Photodesmus blepharus. And if you want to find Candidatus Photodesmus blepharus, the one-fin flashlight fish is the only species on Earth where you’ll find it. The same waters around the Banda Islands are also home to a nearly identical species, the two-fin flashlight fish, with its own bacteria-loaded light organ. But the bacteria glowing inside them is different. Each species of flashlight fish inherits its own exquisitely rare microbial partner.
All species of animals and plants are shot through with microbes, ourselves included. By one estimate, each human being contains about 37 trillion human cells and about the same number of bacteria. It’s easy to ignore our bacterial half, because human cells are hundreds of times bigger than microbes. Yet that’s no reason to ignore them. We have thousands of species of bacteria within us, each carrying thousands of its own genes that are fundamentally unlike our own. In this respect, we are no different from any other animal—any Portuguese man-of-war, any desert scorpion, any elephant seal. We’re not even very different from a sugar maple tree or an evening crocus.
The bacteria we’re most familiar with are those that cause diseases, chewing through our skin and raging through our guts. Yet even in the best of health, we are still rife with permanent lodgers. Some harmlessly cling to their hosts, scavenging molecular scraps. Others perform tasks on which their hosts depend for their survival. If the flashlight fish had no bacteria, it would have no flashlight. Other microbes carry out tasks that are harder to see but no less important. They synthesize vitamins, they nurture a well-tempered immune system, they form a living barrier against dangerous pathogens. The microbiome, as this collective is known, blurs any simple notion of what it means to be an individual organism. If we turned into true individuals, sterilized of our microbiome, we’d become sick and might well die.
In each species, every new generation acquires a microbiome. In some regards, this cycle of renewal looks a lot like heredity. A new animal does not acquire its own genes out of the blue, synthesized from scratch. Its genes have been duplicated over and over again inside the cells of its ancestors, taking an extraordinary journey to get to each new animal. A man, for example, starts off as a zygote full of genes, which are copied each time that fertilized egg divides. The genes end up in totipotent cells, and then in pluripotent cells, and then in cells destined for different tissues. Some of those cells end up as germ cells. As these cells migrate through the body, they bring their genes to the region where the testicles will later develop. Years later, the descendants of these cells may develop into long-tailed sperm, each containing only one copy of each of the man’s genes. Although a man makes billions of sperm over the course of his life, only a tiny fraction of them at most will ever manage to leave his body and enter a woman’s reproductive tract, and fewer still will deliver his genes into an egg.
The genes of bacteria can take strikingly similar routes of their own through the generations of their hosts. One of the most remarkable of these journeys takes place thousands of feet underwater, where thick beds of vesicomyid clams thrive around cracks in the seafloor. The clams soak up hydrogen sulfide—the toxic chemical that gives rotten eggs their awful smell—rising out of the cracks. They absorb it into their muscles, and then their circulatory system delivers the compound to their gills. Special cells in the gills—cells that don’t exist in other species of clams—split sulfur atoms from the hydrogen sulfide molecules, releasing the energy stored in their bonds. The clam uses this energy to combine carbon, hydrogen, and oxygen into sugar molecules. The clams act much like trees, except that they capture a subterranean chemical energy instead of sunlight.
To be precise, it’s not the clams themselves that seize the seafloor’s energy. The specialized cells in their gills are actually bacteria. They carry the gene for an enzyme that can break down hydrogen sulfide. In exchange for this service, the clams supply the bacteria with a well-appointed home. Without those bacteria, the clams would starve; without the clams, the bacteria would barely eke out an existence.
This relationship is remarkable for many reasons, not the least of which is geography. Because vesicomyid clams can grow only where hydrogen sulfide seeps out of the seafloor, clam beds may be miles from each other. The clams broadcast their sex cells into the surrounding water, and after fertilization the clam larvae drift through the sea. Most of them will land in the marine desert and die. Only a few will end up at a site where they can grow. They bring with them the bacteria they need to survive, as their ancestors did.
To understand how the clams manage to hold on to their partners is difficult, because it’s nearly impossible to rear a deep-sea creature in the comfort of a laboratory. Instead, scientists haul up clams from the seafloor and pick apart their dead bodies for clues. In 1993, S. Craig Cary and Stephen Giovannoni of Oregon State University mapped the bacteria inside clams by searching for their DNA. They found some in the gill cells that house the microbes. But they also found some bacterial DNA in the ovary-like organs where clam eggs develop. Somehow the bacteria were traveling through the clams from the gills to the eggs, which they could invade in order to get into the next generation. The new clams are born infected, inheriting an expanded set of genes—some animal and some bacterial.
It’s hard not to wonder what Darwin would have thought of these clams. When he pictured heredity, he saw gemmules streaming from across the body to the germ cells, coming together to carry on the body’s traits to the next generation. His theory of pangenesis turned out to be wrong, and biologists set it aside as one of his exceptional blunders. They turned instead to August Weismann’s stark division between the germ line and the soma. Now researchers are finding that deep-sea clams use a gemmule-like form of heredity to carry their partners into the future.
If these deep-sea clams were the only species on Earth to inherit a vital trait this way, it might be possible to dismiss them as an oddity, in the same way it was once possible to dismiss contagious cancers as a Tasmanian fluke. But they have company. Many animals ensure that essential bacteria get inside their eggs. And some of them—like cockroaches—are a lot easier to study than deep-sea clams.
Among the microbes that live inside cockroaches is one called Blattabacterium. Just like clams, cockroaches develop special cells inside of which Blattabacterium can dwell. Instead of feeding on chemical-laden seawater, cockroaches graze on organic matter on land, able to survive on what they find on the floor of a forest or a New York apartment. Blattabacterium is essential to their global conquest. As the insects eat, they store away nitrogen in an organ in the cockroach abdomen, called the fat body. Inside the fat body are some cells infected with Blattabacterium. The bacteria convert that nitrogen into amino acids and other building blocks that the cockroach needs to grow.
Sometimes the cells housing Blattabacterium will take a trip. They crawl out of the fat body and seek out the cockroach’s eggs. They attach themselves to the eggs for a few days before ripping themselves open. Their resident bacteria spill out, to be swallowed up by the eggs, so that a new generation of cockroaches can continue to conquer the world.
These strictly in-house bacteria—known as endosymbionts—did not always live this way. Their ancestors lived outside of hosts. The free-living cousins of endosymbionts have helped researchers learn about how some bacteria have evolved into such intimate partners. In case after case, the microbes took a gradual slide into a life inside.
This research shows that when the free-living ancestors of endosymbionts came into contact with a host—be it a roach, a clam, or one of millions of other species—they could grow on it by good fortune, or even inside it. By sheer coincidence, these bacteria provided some benefit to their hosts—perhaps casting off a useful amino acid in their waste. If their hosts did well as a result, the bacteria had more opportunity to reproduce in them. Natural selection favored bacteria that could do their hosts more favors because their interests were becoming aligned. Likewise, their hosts evolved to nurture the bacteria. Evolving special cells to shelter the bacteria ensured that animals could enjoy their services.
As the bacteria grew ever more pampered, genes that were once essential in the outside world became useless. Mutations that broke these newly superfluous genes no longer guaranteed extinction. The bacteria became genetically streamlined, their genomes shrinking in size by 90 percent or more. Some endosymbionts have lost the ability to do just about anything except the one thing that their host can’t do.
Both the bacteria and their animal hosts became trapped in an evolutionary rabbit hole from which there is no escape. Once they were locked in symbiosis, their evolution began to follow identical paths. When an insect species split in two, its endosymbionts split as well. Their evolutionary trees became mirror images, with identical branches splitting from each other for tens of millions of years.
The story of the one-fin flashlight fish is a lot like those of the clams and the cockroaches. It also builds a special shelter—the light organ—where its bacteria can thrive. Every new generation of flashlight fish inherits a fresh supply of the same species of bacteria. In effect, the fish are expanding their genomes to include light-producing genes. Those genes just so happen to belong to a separate species. As the bacteria have adapted to life inside light organs, they have lost 80 percent of their genome.
There is one important difference, however. A female flashlight fish does not carefully move bacteria inside her body, transferring them from her light organ into her eggs. Her offspring hatch from their eggs lacking the microbes they need to glow. To gain their own flashlight, they have to get infected.
Each day, as an adult one-fin flashlight fish hunkers down in a cave, it sheds some of its bacteria. While Candidatus Photodesmus blepharus has lost most of the genes required to live outside an animal, it still clings to a few. Some of the genes enable it to build tails it can whip back and forth to swim through the sea. It also still retains genes for making chemical-sensing proteins, which it likely uses as a molecular nose, sniffing its way to young flashlight fish that it can invade. Ultimately, though, it’s up to the fish to let the bacteria into their light organ. They’ve got a strict admission policy: The same waters also teem with the bacteria that give light to the two-fin flashlight fish, but those microbes can’t get in.
This pattern of heredity is looser than the strict transmission of bacteria in clams and cockroaches. And yet it still embodies some of heredity’s essential features. In the journey from one generation to the next, the bacteria and their genes aren’t neatly bundled together with the host’s genes in an egg. But the outcome is the same: A combined genome continues to produce a cream-colored light in the Banda Sea in each new generation, as it has for millions of years.
Our own microbiome is yet another step away from standard heredity. We don’t develop a special pouch that exists only to be packed with one species of bacteria. If you give antibiotics to a vesicomyid clam and destroy its sulfur-feeding bacteria, it will die. But there’s no single species of bacteria upon which our own life depends. In fact, there’s not even a single species of bacteria that we humans all share. We house personalized zoos.
I got an intimate appreciation for our variety a few years ago when I went to a science conference. Wandering from talk to talk, I encountered a biologist named Rob Dunn who waved a Q-tip in front of me. He asked if I’d give him a sample from my belly button for a survey he was carrying out. I am the sort of person who says yes to such requests without missing a beat, and so within a few minutes I was in the nearest men’s room, knocking out lint from my navel and swiping it with Dunn’s Q-tip, which I dropped into a plastic vial of alcohol.
Dunn and his colleagues collected hundreds of these vials and extracted DNA fragments out of each of them. Most of those fragments were obviously human. But some belonged to bacteria. Dunn and his colleagues searched for matching sequences in online databases to figure out which species they came from. In my belly button, they found fifty-three species of bacteria. When Dunn sent me a spreadsheet with my personal navel catalog, he added a message. “You, my friend, are a wonderland.”
Having fifty-three species of bacteria in one’s navel is nothing special, I should point out—Dunn and his colleagues have found twice as many in some other people. To get an overall sense of this diversity, the scientists analyzed results from sixty people. All told, they identified 2,368 species. None was present in every person. Eight species were present in at least 70 percent of Dunn’s subjects. But 92 percent could be found only in 10 percent or less of the subjects. The majority was found only in a single person. When I looked over my spreadsheet, I could see that seventeen of my species were unique to me. One type, called Marimonas, had only been known from the Mariana Trench, the deepest spot in the ocean. Another, called Georgenia, lives in the soil. In Japan.
On discovering this, I e-mailed Dunn to let him know I’d never been to Japan.
“It has apparently been to you,” he replied.
The weirdness of my spreadsheet stems from our profound ignorance of the microbial world. Microbes are unimaginably diverse, with thousands of species in a single spoonful of soil. Although microbiologists have been naming species of bacteria for well over a century, they’ve described only a tiny fraction of the Earth’s single-celled diversity. Marimonas was named for a deep-sea microbe, but the lineage likely includes many other species adapted to other environments, including human skin.
Within the howling complexity of the human microbiome, however, you can still hear heredity’s signal. It begins when a mother seeds her children’s microbiome. When this seeding starts is still not clear. Although researchers have long held that embryos start off sterile, in a bacteria-free amniotic sac, a few studies have hinted that at least some maternal bacteria may slip into the fetal sanctuary. What is abundantly clear, however, is that once a baby starts moving down through the birth canal, it gets contaminated. The bacteria growing on the canal walls slather the baby in a microbial coat. Some of the bacteria grow across its skin, while some slip into the mouth and make their way to the gut.
A nursing mother can inoculate her baby with even more bacteria. Breasts foster microbes, which they allow to mix into their milk. Small-scale studies suggest that the strains that move most successfully through nursing into the babies are especially good at breaking down milk sugar and converting compounds in milk into vitamins that babies need. Mothers appear to play favorites, promoting certain species of bacteria in their babies and filtering out others. While breast milk contains a lot of nutrients that a baby can absorb, it also contains certain sugars, called oligosaccharides, that are indigestible. Indigestible by humans, to be specific. Certain strains of gut bacteria delight in oligosaccharides, multiplying in the guts of nursing infants. Mothers may thus transmit microbes to future generations in a heredity-like way.
To see how closely our microbes have followed us through the generations, a University of Texas microbiologist named Howard Ochman and his colleagues looked far back in evolutionary time. They compared the microbiomes of humans and those that live in our closest primate relatives: gorillas, chimpanzees, and bonobos. (Bonobos are a species of ape that split from the ancestors of chimpanzees about two million years ago.) They found that many lineages of bacteria that live in the human gut do not exist in the guts of our fellow apes. Instead, those apes have their own related strains of bacteria.
When Ochman and his colleagues compared the evolutionary trees of the hosts and the bacteria, they lined up closely, branching in the same patterns. Microbes in chimpanzees tend to be more closely related to ours than those that live in gorillas—just as chimpanzees themselves are our closest kin. Ochman’s study suggests that for more than fifteen million years, our ancestors have been in a tight coevolutionary dance with their microbiome.
As hominins split off from other apes, they adapted to new kinds of diets, and their microbes may have adapted as well. Our ancestors evolved ways to foster only the strains of bacteria that belonged to us and not to other species. The oligosaccharides in human milk are different from those in the milk of other mammals. They may be adapted to foster some of our own strains of bacteria, shutting out others that can grow in other species.
In a few cases, bacteria get passed down so loyally from human parents to children that they can serve as rough genealogical records. A species known as Helicobacter pylori adapted long ago to life in the human stomach. Impervious to the digestive juices we make, it guzzles glucose in the food we eat. How a microbe can get from one human stomach into another is a mystery, but epidemiological studies show that infections with H. pylori start early in childhood. The bacteria have been found in the plaque on people’s teeth, carried there by refluxes into their mouths. It’s possible that mothers and other family members infect babies by transmitting the bacteria from their mouths to the children.
Whatever route H. pylori takes, it’s a tremendously successful one. By some estimates, it lives in the stomachs of over half the people on Earth. Before the advent of antibiotics, that figure might have been closer to 100 percent. A small fraction of people who carry the bacteria will go on to develop ulcers and gastric cancer, but H. pylori is, for the most part, our friend. It sends signals to the developing immune system in children, helping it learn how to respond carefully to threats rather than overreacting and harming our own bodies. In billions of people’s stomachs, the microbe grows and divides. The mutations that it accumulates along the way have allowed scientists to draw an evolutionary tree of the bacteria.
The history recorded in its branches bears a striking resemblance to the history of our own species. H. pylori first colonized humans in Africa more than 100,000 years ago, and people carried it around the world with them. If you want to know something about your ancestry, you can look at your own genes. But you can also get some clues from the H. pylori that you inherited from your ancestors.
Children do not inherit all their microbes only from their mothers, or even just their families. They can pick up bacteria from friends’ toys they stick in their mouths, from teachers who wipe the dirt off their cheeks, even from the air they breathe. Yet even the bacteria that move freely from stranger to stranger also become intertwined with our own heredity.
To see this intertwining, you first have to think about our microbiomes as a heritable trait, just like our height, intelligence, and risk of getting a heart attack. And you have to study it as such. Julia Goodrich, a microbiologist at Cornell University, and her colleagues did just this, investigating the microbiomes of twins to see how their genetic similarities influenced the species they carried.
The scientists collected stool samples from 1,126 pairs of twins and cataloged the microbial inhabitants. Out of thousands of species of bacteria, they identified twenty that were more strongly correlated in identical twins than in fraternal ones. In other words, if one identical twin carried a particular species, the other twin was more likely to carry it, too. The scientists found that some species were more heritable than others. The most heritable of all was a kind called Christensenella. Goodrich and her colleagues estimated its heritability at around 40 percent. That’s on par with moderately heritable traits, such as anxiety.
These results suggested that the genes we inherit from our parents help determine which microbes we end up harboring. To investigate this possibility further, Goodrich and her colleagues took a different approach: They scanned people’s genomes, looking for people who shared certain variants and certain kinds of bacteria. They discovered that people with one variant have a high population of microbes belonging to a group of species called bifidobacteria.
The nature of that genetic variation hints at why it favors bifidobacteria. It controls a gene for a protein we use to break down a sugar called lactose. Babies make lots of this protein—called lactase—to break down the lactose in breast milk. The majority of children stop making lactase as they shift to eating solid food. But others have a different genetic variant that lets them continue making lactase, allowing them to digest milk sugar into adulthood.
Bifidobacteria thrives on the lactose that doesn’t get digested by the time it reaches the large intestine. People who can take it up tend to have fewer bifidobacteria. But those who shut down their lactase wind up feeding a bigger population of microbes.
It’s not so clear why Christensenella, the most heritable bacteria of Goodrich’s study, is heritable. Perhaps that mystery has something to do with the fact that the microbe was only discovered in 2012. Scientists have determined that Christensenella breaks down a variety of sugars, and other types of bacteria feed on its by-products.
There are hints that Christensenella acts like a gatekeeper, helping to control how much of the energy in our food actually gets to our body instead of to our microbiome. One clue comes from looking at who carries Christensenella and who doesn’t: Lean people are more likely to carry it than overweight ones. Another clue emerged from an experiment Goodrich and her colleagues ran on mice. They infected baby mice with Christensenella and then waited for them to grow to adulthood on a regular diet. The bacteria left the animals slim. Mice without Christensenella put on 15 percent more weight and ended up with 25 percent body fat. Mice with Christensenella gained only 10 percent more weight and reached 21 percent body fat.
These findings raise the possibility that we have to take the microbiome into account to understand why a trait such as weight is heritable. Some of the genetic variants behind the heritability of weight may not directly influence how our cells store fat. Instead, we inherit a variant that fosters Christensenella in our guts. It’s the bacteria that take it from there.
There is one species of bacteria that has merged snugly into our bodies—even more snugly than the microbes that give the flashlight fish its light. This microbe has actually merged into our heredity, becoming such an intimate part of our existence that for decades many scientists refused to believe it started out as a free-living organism. I’m speaking of mitochondria, the tiny pouches that produce fuel inside our cells.
Mitochondria first came to the attention of biologists in the late 1800s as they developed new chemicals for staining the interior of cells. The stains revealed that the cells of animals were packed with mysterious granules. A German biologist named Richard Altmann published an entire book on these strange objects, filled with loving drawings of extraordinary accuracy. Altmann was astonished by how much the granules looked like bacteria. Not only were they shaped like bacteria, but sometimes Altmann’s stains revealed them dividing in two like bacteria. Altmann developed an obsessive conviction that these granules were alive. He called them “elementary organisms.” Altmann believed that cells themselves came into existence when these granules assembled into colonies and built a shelter of protoplasm around themselves.
The idea sounded absurd to other biologists. They rejected it so completely that Altmann turned into a bitter recluse. He would slip in and out of his lab through a back door, avoiding all human contact. His colleagues began referring to him as “the ghost.” In 1900, Altmann died under mysterious circumstances at age forty-eight.
“Things went from bad to worse,” the biologist Edmund Cowdry wrote cryptically in a 1953 history of mitochondrial research, “and the end was tragic and of the sort expected.”
Cowdry forgave Altmann his error about mitochondria, “for the similarities between them and bacteria really are remarkable,” he said. Ultimately, though, Cowdry and most other researchers judged the similarities only superficial. Mitochondria were simply parts of the cell, their construction encoded by the cell’s own genes.
Years of subsequent research revealed that mitochondria performed an essential job: They use oxygen and sugar to create a cell’s fuel supply. Researchers also discovered that mitochondria were shared not only by all animals but also by plants, fungi, and protozoans—in other words, by all eukaryotes. Tracing these lineages on the tree of life revealed that mitochondria must have evolved in the common ancestor of eukaryotes, some 1.8 billion years ago.
In the early 1960s, an astonishing fact about mitochondria came to light: They contained more than just proteins. Scientists also discovered they store their own DNA—if only a little. Human mitochondria have only thirty-seven genes, compared to about twenty thousand protein-coding genes in the nucleus. Nevertheless, the discovery of mitochondrial DNA baffled scientists. Our cells have many compartments—lysosomes for breaking down food molecules, for example, and the endoplasmic reticulum for moving proteins around the cell. But of them all, only mitochondria have their own set of genes.
Lynn Margulis, a biologist at the University of Massachusetts, argued that there was only one way to make sense of the discovery: It was time to revisit the old theories of Altmann and other early cell biologists. The evidence pointed to mitochondria starting out as free-living bacteria, and still holding on to a few of their original genes.
Margulis would be proven right. Starting in the 1970s, scientists began sequencing mitochondrial DNA. When they looked for the most similar genes in other species, they found that mitochondria most resembled bacteria. They were even able to narrow the genetic resemblance down to one lineage in particular, a group of species called alphaproteobacteria.
Before gaining their mitochondria, the evidence now suggests, our ancestors were microbes that survived by slurping some kind of molecular debris from their surroundings. About 1.8 billion years ago, a small species of bacteria—an alphaproteobacteria, to be specific—ended up permanently inside of them. Living alphaproteobacteria have given scientists inspiration for ideas about how this merger happened. Some researchers have argued that the alphaproteobacteria slipped into the larger cells as parasites. Their host did their best to destroy the invaders, but the alphaproteobacteria evolved defenses. In time, they stopped spreading from cell to cell. When their host divided, the alphaproteobacteria wound up in both the daughter cells.
Other scientists have proposed that the two microbes lived side by side at first. They traded essential nutrients, helping each other thrive. The closer they were to their partners, the more reliably they could exchange these gifts. Eventually, they merged entirely.
Whichever is the case, gaining mitochondria marked one of the great leaps in the evolution of life. A cell now could harvest the fuel made by its new lodgers. The more mitochondria a cell could house, the more energy it could use. This symbiosis spiraled upward, allowing eukaryote cells to become far bigger, far more complex, than any cell before. Instead of feeding on molecular debris, eukaryotes now had enough fuel to chase after bacteria and engulf them. Later, these single-celled predators began clinging together, evolving into multicellular creatures.
Ensconced in their new home, mitochondria followed the same path that endosymbionts so often do. They abandoned many of the genes they had once needed to live freely on their own. Yet mitochondria never gave up their own form of heredity. Altmann might have been wrong to think that mitochondria were independent life-forms. But he was right to think of bacteria when he saw mitochondria dividing. Within a cell, a mitochondrion will sometimes split in two, and the daughter mitochondria inherit copies of its DNA, just as their free-living ancestors did nearly two billion years ago.
When our own cells divide, their daughter cells inherit a portion of their mitochondria, which keep dividing over the course of our lifetime. Our bodies don’t get overrun by mitochondria because our cells sometimes destroy them, keeping their numbers in check. Our deaths bring an end to the lineages of mitochondria in our bodies; the only ones with a chance to escape to the future are those that dwell in women’s eggs. A man’s mitochondria have no future, because their sperm destroy them during fertilization.
The fact that mitochondria are inherited only down the maternal line makes their DNA a powerful genealogical tool. It allowed some scientists to reunite the family of the Tsar Nicholas. It allowed others to reunite all living humans, tracing our mitochondrial DNA to a single woman in Africa 150,000 years ago. Yet mitochondria’s distinctive patterns of heredity have also created deep confusion.
When mitochondria copy their DNA, they can make mistakes and introduce mutations. Some of those mutations can disrupt their fuel-generating assembly line, while others can cause devastating hereditary diseases. They can make eyes go blind, ears go deaf, muscles waste away. Many of these mitochondrial diseases went overlooked for decades by geneticists, because they flouted Mendel’s Law. In some families, a disease will only sporadically strike relatives over the generations. In other families, the same disease will reliably occur in every child of a mutation-carrying mother.
It wasn’t until the late 1980s that scientists began pinpointing the genetic basis of mitochondrial diseases. Since then, they’ve identified hundreds of these disorders, which together afflict one in four thousand people. Strangely, though, these people often have relatives who carry the same mutations in their mitochondria but don’t suffer the same symptoms.
This confusion dissolves when you bear in mind that mitochondria are our resident bacteria, following their own rules of heredity. If a single mitochondrion mutates, the cell that carries it will continue functioning normally, because it still has hundreds of other healthy ones. When the cell divides, one of its daughter cells inherits that one mutant mitochondrion. As the mutant mitochondrion itself divides, it becomes a bigger burden on cells. When the number of mutant mitochondria rises above a certain threshold, a cell will start to fail.
Mutant mitochondria can continue to become more common from one generation to the next. A woman with low levels of mutant mitochondria may give birth to children who cross the threshold into a full-blown mitochondrial disease. Thanks to chance, some of her children may get sick, while others remain healthy.
Studying mitochondrial diseases may eventually lead scientists to an answer to the biggest question about their heredity: Why does it follow only the maternal line? We all need mitochondria, males and females alike, to stay alive. Sperm need mitochondria to power their swim toward conception. Scientists have discovered a few species in which both parents pass down their mitochondria to their offspring. Ink cap mushrooms are one. Geraniums are another. In mussels, sons inherit mitochondria from both parents, while daughters inherit them only from their mothers. But in the overwhelming majority of species, fathers never pass down their mitochondria.
All these clues hint that there must be some powerful advantage to limiting mitochondria to the maternal line. It’s possible that this kind of heredity evolves because mixing together mitochondria from two parents can be a disaster for children. In 2012, Douglas Wallace, an expert on mitochondrial diseases at the University of Pennsylvania, and his colleagues injected mitochondria from one healthy line of mice into the cells of a genetically distinct line. They then used those blended cells to produce mouse embryos. When the animals became adults, they suffered a host of problems, especially in their behavior. The mice became stressed-out, lost their appetite, and did badly at learning their way out of a maze.
Limiting mitochondrial heredity to one parent may help organisms move ahead in the evolutionary race. And once a species restricts mitochondria to eggs, mothers sometimes evolve ways to inspect their eggs, eliminating ones with too many mutations. The bacteria that sometimes infected our ancestors have now become so much a part of our heredity that their quality is the standard by which new human lives can come into existence.