She Has Her Mother's Laugh: The Powers, Perversions, and Potential of Heredity (55 page)

BOOK: She Has Her Mother's Laugh: The Powers, Perversions, and Potential of Heredity

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
, had only been known from the Mariana Trench, the deepest spot in the ocean. Another, called
, 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.
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
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
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
breaks down a variety of sugars, and other types of bacteria feed on its by-products.

There are hints that
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
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
and then waited for them to grow to adulthood on a regular diet. The bacteria left the animals slim. Mice without
put on 15 percent more weight and ended up with 25 percent body fat. Mice with
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
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.

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