Genes, Natural Selection, and Evolution in Action

The puzzle of heredity–how two people can create a child with qualities of both parents–inspired a lot of wild ideas in the 1800s. One of the wildest, at least from our perspective today, was known as pangenesis. It held that heredity is carried by tiny particles that bud from cells throughout a person’s body. These particles (called gemmules) supposedly stream like trillions of migrating salmon to the sex organs, where they concentrate inside sperm or eggs. And when a sperm fertilizes an egg, the gemmules of both parents blend together. Since each particle comes from a cell from a particular part of a parent’s body, they combine together into a new person with traits of both parents.

Pangenesis turned out to be a failure, but the scientist who proposed it was not relegated to history’s ranks of scientific crackpots. His reputation survived, thanks to a few other ideas that have withstood the test of time. Pangenesis was the work of Charles Darwin.

Along with Earth’s age, heredity was one of Darwin’s great frustrations. Origin of Species persuaded most scientists by the end of the nineteenth century that evolution was a reality, but many of them were skeptical of Darwin’s own mechanism of change, namely, natural selection. Many of them resurrected Lamarck’s old ideas instead. Perhaps there was a built‑in direction to evolution, they claimed, or perhaps there were ways that adults could acquire traits in their lifetimes that they could pass on to their children. If Darwin could have shown that heredity forbids these ideas but allows for natural selection, he could have refuted his critics. But that knowledge was beyond Darwin and all the other scientists of his day.

In the years after Darwin’s death, biologists finally began to learn how heredity works. Only then could they recognize that the neo‑Lamarckians were wrong. Only then could they recognize how heredity makes natural selection not just possible but inevitable and how it allows new species to form. It took the work not just of geneticists to make this discovery, but of zoologists and paleontologists as well. By the middle of this century, they had combined their research into a collective understanding of evolution that became known as the “modern synthesis.” Younger scientists have used the modern synthesis as the foundation for their research. They’re beginning to understand how evolution happens on a molecular level, and as a result, natural selection is no longer the elusive, imperceptible force Darwin imagined it to be. In fact, scientists can witness natural selection happening in the wild today, as well as the branching of old species into new ones. Scientists don’t even have to watch animals or plants or microbes to see natural selection play out: they can watch it take place within our bodies, or even among artificial life‑forms within a computer.

Heredity’s Monk

If history had played out differently, scientists might have cracked the secrets of heredity in Darwin’s own lifetime. Even as he was writing Origin of Species, a Moravian monk was already discovering the fundamental laws of genetics in his garden.

Gregor Mendel was born to a poor peasant farmer in 1822 in what is now the Czech Republic and grew up in a two‑room house. When his teachers recognized Mendel’s quick intelligence, they arranged for him to become a novitiate at the monastery in Brno, then in Moravia. The monastery was filled with monks as dedicated to science as to prayer, who read deeply in geology, meteorology, and physics. From the monks, Mendel learned about the latest advances in botany, such as new techniques for artificially fertilizing plants in order to breed better and better strains. Eventually they sent Mendel to the University of Vienna, where he continued to study biology. But it was the physics and mathematics that he learned there that shaped him as a scientist. The physicists in Vienna showed Mendel how to test a hypothesis with experiments–something that few biologists at the time were doing. The mathematicians meanwhile taught Mendel how to use statistics to find order hidden in seemingly random collections of data.

In 1853 Mendel came back to Brno. He was by now a man in his thirties, broad‑shouldered and a little corpulent, with a high forehead and twinkling blue eyes behind gold‑rimmed glasses. He worked as a schoolteacher, teaching natural history and physics to second and third graders. Although he had 100 students and six days of classes a week, he still managed to live the life of a scientist, taking regular readings of the weather and keeping up with scientific journals. And during that time he decided to set up an experiment to learn about the heredity of plants.

In Vienna, some of Mendel’s professors struggled to understand what made species distinct, about how one generation produced a new generation that looked like itself. These questions fused together in the mystery of hybrids. Breeders knew how to develop distinct varieties of flowers, fruits, and other plants, and they could cross varieties to produce hybrids. Many were sterile, and among the hybrids that could produce offspring, the new generations often reverted back to the forms of their ancestors. But if plants could somehow form stable hybrids, it was possible that species were not eternal or unchanging. In the 1700s, the Swedish biologist Carl Linnaeus had speculated that species of plants belonging to the same genus had developed from a common ancestor by hybridization.

For most of the nineteenth century, scientists generally thought that heredity worked by blending the qualities of parents in their offspring. But Mendel came up with a radically different idea: parents could pass down traits to an offspring, but their traits did not blend. To test his idea, Mendel planned out an experiment to cross varieties of plants and keep track of the color, size, and shape of the new generations they produced. He chose peas, and for two years he collected varieties and tested them to see if they would breed true. Mendel settled on 22 different varieties and chose seven different traits to track. His peas were either round or wrinkled; yellow or green. Their pods were yellow or green as well, and they were also smooth or ridged. The plants themselves might be tall or short, and their flowers might blossom at their tips or along their stems. Mendel would record the appearance of the traits in each generation.

Delicately placing the pollen of one plant on another, Mendel created thousands of round‑wrinkled pea hybrid seeds. He then waited for the plants to bloom in the monastery garden. When he shucked the pods a few months later, he saw that the hybrid peas were all round. The wrinkled trait had utterly disappeared from sight. Mendel then bred these round hybrids together and grew a second generation. Some of their offspring were wrinkled (and just as deeply wrinkled as their wrinkled grandparents). The wrinkled trait had not been destroyed in the round generation; it had gone into hiding in the hybrids and then reappeared.

The number of peas that ended up wrinkled would vary on each plant, but as Mendel counted up more and more of them, he ended up with a ratio of one wrinkled seed for every three round ones. He crossed varieties to follow the fate of other traits, and the same pattern emerged: one green plant for every three yellow ones, one white seed coat for every three gray ones, one white flower for every three violet ones.

Mendel realized that he had found an underlying regularity to the confusion of heredity, but contemporary botanists pretty much ignored his work. He died at his monastery in 1884 with a reputation as little more than a charming putterer. But he was actually a pioneer in genetics, a field that didn’t even come into existence until 16 years after his death. After a hundred years of research, it is now clear why Mendel’s peas grew the way they did.

Peas, like every other organism on Earth, carry in each of their cells a molecular cookbook for creating their bodies. This information‑bearing molecule is called deoxyribonucleic acid, better known as DNA. It is shaped like a twisted ladder; its information is inscribed on its rungs, made from a pair of chemical compounds known as bases. Bases serve as the letters in life’s recipes, but unlike the 26 letters of the English alphabet, DNA is written with only 4–adenine, cytosine, guanine, and thymine.

A gene–a stretch of DNA usually spanning a few thousand base pairs–is a recipe for a protein. To create a protein, our cells construct a single‑stranded version of a gene (called RNA), which gets shuffled to a protein‑building compartment. Proteins are long molecular chains, as are DNA and RNA, but they are not made out of bases. Instead, proteins are formed from another group of compounds called amino acids. Our cells use the information encoded in the bases of RNA to grab the appropriate amino acids and assemble them into a chain; once a piece of RNA has been read to its end, the new protein is complete. The attraction of the atoms in the new protein to one another make it collapse, like spontaneously folding origami. Because they take on thousands of different structures, proteins can play thousands of roles, from serving as pores in cell membranes to stiffening fingernails to carrying oxygen from the lungs through the bloodstream.

It is the way the DNA cookbook is passed down from one generation to the next that creates the 3‑to‑l ratio Mendel discovered in his peas. In plants and animals, the recipes of the genes are organized into volumes, each of which is called a chromosome. We humans, for example, have 25,000 genes arranged on 23 pairs of chromosomes. A pair of chromosomes may carry identical versions of a given gene, or they may bear different ones. When a normal cell divides in two, both new cells get a complete collection of genes. But when cells give rise to sperm or egg, each sex cell only receives a single chromosome from each pair. Which of the two it receives is a matter of chance, and when a sperm fertilizes an egg, the two sets of chromosomes unite into a new pair, creating the genetic code for a new organism.

The colors of Mendel’s pea plants, their textures, and all the other traits he recorded were controlled by different versions of pea genes. One of the genes that his peas inherited comes in two different versions, one making them smooth, the other wrinlded. A purebred smooth pea carries two copies of the smooth gene; two copies of the wrinkle‑causing gene can be found in purebred wrinkled peas. When Mendel crossed these breeds of peas together, he got hybrids, each carrying one smooth gene and one wrinkled gene, but bearing a smooth coat. For reasons that geneticists still don’t fully understand, genes like the one that makes peas smooth can dominate their partners.

But while the wrinkled gene was silenced in the hybrids, it did not disappear. Each of the hybrid’s eggs and pollen grains received only one form of the gene, so each offspring had a 50‑50 chance of inheriting a particular gene from each of its parents. Thanks to these odds, a quarter of the new peas received two wrinkled genes, a quarter received two smooth ones, and half received one of each. Because the new hybrids were also smooth, in the second generation the wrinkled peas were outnumbered 3 to 1.

The way most traits are inherited is a lot more complicated than what Mendel recorded when he grew his peas. Very often, a species carries many more than two different versions of a gene. And it is rare that a single gene is alone responsible for a trait. In most cases, many different genes are involved. The human race isn’t divided into those who carry a “tall gene” that makes them 6 feet tall and those with a “short gene” that makes them only 5 feet. Many genes help determine a person’s height, so changing just one of them will make only a slight difference. If our DNA is a cookbook, our bodies are a smorgasbord. Using salt instead of yeast in the bread will make a big difference to the meal, but confusing thyme and oregano in the chili probably won’t raise an eyebrow.