Adapted from “She Has Her Mother’s Laugh: The Powers, Perversions, and Potential of Heredity,” published Tuesday by Dutton, an imprint of Penguin Random House.


ome families are ambushed by blindness. The children in these families are born with eyes that seem perfectly normal. But when they become young adults, some of them suddenly get blurry vision. In a matter of weeks, their central field of view may go completely dark.

The first doctor to notice this disease was Theodor Leber. In 1871, he described four families it plagued. The condition came to be known as Leber hereditary optic neuropathy. Yet even though “hereditary” was part of its name, the disease flouted heredity’s ordinary rules.


It could blind men and women alike, but when researchers drew up pedigrees of families with Leber hereditary optic neuropathy, they found that men could not pass the disease down to later generations. As for women, they passed it down in a baffling manner. Sometimes all their children lost their sight. Sometimes only one child did. Some children in a family might become profoundly blind while others only suffered blurry vision. And the daughters with blurry vision might have children of their own who went on to become suddenly blind.

Scientists spent over a century trying to make sense of the disease. And what they discovered has helped shape our understanding of the way in which heredity works.

Heredity cannot always be explained by the 23 chromosomes of DNA in our cells. Our cells are also home to ancient lodgers — bacteria that invaded the cells of our ancestors 1.8 billion years ago, with DNA of their own. These microbial residents, known as mitochondria, have become essential parts of our own biology. But even today, they play by their own hereditary rules.

We generally don’t give much thought to the bacteria that call us home. Yet, like all species of animals and plants, we are shot through with microbes. By one estimate, each human being contains about 37 trillion 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.

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 53 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 53 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. But when I looked at my 53 species, I was astonished by their diversity. The spreadsheet I was given laid out information on where else my bacteria have been found. 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 emailed Dunn to let him know I’d never been to Japan.

“It has apparently been to you,” he replied.

Bacteria built to adapt


he weirdness of my spreadsheet stems from our profound ignorance of the microbial world. Thousands of species of microbes can live 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.

We can acquire many of these bacteria from our environment: from dirt, handshakes, doorknobs, and computer keyboards. Yet our inner menagerie is not simply a random sampling of the microbial traffic flowing around us. Many of these species have adapted to our human habitat over millions of years. They’ve evolved tricks for finding food in our nooks and crannies. Our own bodies have adapted to them as well, able to recognize them as friends rather than enemies. And it’s possible that some members of the human microbiome have evolved intimate ways to get from one generation to the next.

When Dunn sent me a spreadsheet with my personal navel catalog, he added a message. “You, my friend, are a wonderland.”

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.

Other species appear to have found an even more intimate route from mother to child. The tissue in human breasts is home to a select group of bacteria. When mothers nurse their babies, some of those bacteria can get mixed into the 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 also seem 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 by humans. By contrast, certain strains of gut bacteria delight in oligosaccharides, multiplying in the guts of nursing infants.

Researchers have also discovered that the oligosaccharides in human milk are different from those in the milk of other mammals. They may have adapted to foster some of our own strains of bacteria, shutting out others that can grow in other species. Mothers may thus transmit microbes to future generations in a heredity-like way.


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Even at birth, babies are already inoculated. Precisely when this seeding begins is still not clear. A few studies have hinted that at least some maternal bacteria may slip into the amniotic sac and colonize the fetus. What is abundantly clear, however, is that once a baby starts moving through the birth canal, it becomes decidedly unsterile. The bacteria growing on the canal walls slather the baby in a microbial coat. Some of the bacteria grow across its skin, while others slip into the mouth and make their way to the gut.

It’s possible that scientists will someday discover some species with even more intimate links to our own heredity. After all, they’ve barely started to catalog the thousands of species that make up the human microbiome. And we know that in other species of animals, bacteria have merged even more with their hosts.

She Has Her Mother's Laugh
Courtesy Dutton

In the waters off the Banda Islands, an archipelago in Indonesia, one such species lights up the ocean. The one-fin flashlight fish (Photoblepharon palpe­bratus) 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, a pair of jellybean-shaped organs emits a cream-colored light.

(The fish can use the light 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.)

But the light produced in those organs comes from bacteria, not fish cells. 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.

One-fin flashlight fish hatch from their eggs lacking the microbes they need to glow. To gain their own flashlight, they have to get infected.

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 they whip back and forth to swim through the sea. It uses chemical-sensing proteins to sniff out 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.

As they’ve adapted to life with their hosts, these microbes have lost 80 percent of their DNA. They’ve only held onto a bare-bones collection of genes they need to find new hosts (encoding traits such as tails and microbial noses), and to provide nutrients to the fish. Their fish hosts take care of the rest of their needs.

‘Elementary organisms’


he one-fin flashlight fish helps expand our vision of the microbiome. Instead of wayward bacteria that happen to wind up inside their hosts’ bodies, they can become an integral part.

Our mitochondria — the tiny, fuel-producing pouches inside our cells — fit that bill.

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.

Researchers judged the similarities between mitochondria and bacteria as 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 — one of the main branches of life, known as eukaryotes. Mitochondria must have evolved in the common ancestor of eukaryotes, some 1.8 billion years ago.

But 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.

The discovery 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 ended up permanently inside of them.

The closest relatives of mitochondria have given scientists inspiration for ideas about how this merger happened. Some researchers have argued that the ancestors of mitochondria slipped into larger cells as parasites. Their host did their best to destroy the invaders, but the bacteria evolved defenses. In time, they stopped spreading from cell to cell. When their host divided, the bacteria 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 the partners lived next to each other, the more reliably they could exchange these gifts. Eventually, they merged entirely.

Whichever scenario actually happened, the origin of mitochondria marked one of the great leaps in the evolution of life. Cells now could harvest the fuel made by their 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 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 2 billion years ago.

Yet when mitochondria copy their DNA, they can make mistakes and introduce mutations. In 1988, Douglas Wallace, now at the University of Pennsylvania, and his colleagues discovered that people with Leber hereditary optic neuropathy all share the same mutation in their mitochondrial DNA. In the three decades since, researchers have discovered hundreds of other hereditary mitochondrial diseases, causing a huge range of symptoms. Together, they afflict one in 4,000 people.

The confusing heredity of mitochondrial diseases 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. It seems bizarre for these sperm to destroy their own mitochondria right before conception.

It’s possible that this kind of heredity evolves because mixing together mitochondria from two parents can be a disaster for children.

In 2012, Wallace 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 infected our ancestors have now become so much a part of our heredity that their quality is the standard by which humans can come into existence.

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  • so why can’t ACOG understand the benefit of vaginal seeding? Genome magazine discussed this in an interview with Dr. Rob Knight in Genome magazine. Is no one listening to these amazing discoveries?

  • I maybe totally off track here but I’m curious. I inherited a DNA mutation from my father that is part of the mitochondria, SDHB mutation is Complex II of the Krebs Cycle. My father and his sister died of paraganlioma tumors and I have gastrointestinal tumors . . . Caused by this break in the Krebs Cycle. I have a brother with this same mutation but no cancer. My instinct is that my one good allele from my mother was broken by exposure to black mold. This cancer is usually first seen in teens and young adults such as my father’s case although sometimes it occurs in babies . . . Born with a mitochondrial disease . . . How does this fit into the author’s theory?

  • Why is it considered a mystery that mitochondria follow the maternal line? My understanding of mtDNA is that the egg’s mitochondria is preserved in the egg while the sperm’s mitochondria as part of the tail is discarded upon entry to the egg. Is this incorrect? No man’s mtDNA is transmitted ever as far as I know. Please send me a reference if I am incorrect. Thank you.

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