Survival of the Sickest: Chapter 6 Summary & Analysis

At the end of the 18th century, a doctor in Gloucestershire, England named Edward Jenner discovered a pattern: milkmaids who caught cowpox seemed resistant to smallpox. He scraped a cowpox sore from a milkmaid and purposefully infected teenage boys, who as a result were protected from smallpox. This became the first vaccine, and the word actually comes from the Latin name for cowpox, vaccinia.

Today, we know more about how vaccination works: modern vaccines introduce a harmless version of the virus into our bodies, stimulating our immune system to produce antibodies tailored to defend against the virus. But for a long time, scientists didn’t understand how our bodies created antibodies to fight against every microbial attacker because we couldn’t have enough genes dedicated to each one—until they recognized that genes could change.

When a sperm and egg cell combine to form a zygote cell, all of the DNA needed to build a human being is already in place—the instructions are carried in 3 billion pairs of nucleotides, which amount to fewer than 30,000 genes. These genes are organized into 23 chromosomes, which carry the same type of instructions in each person but with individualized content (say, for hair color or eye color). Every cell in the body contains the same DNA, except for sperm and egg cells—which contain only one set of 23 chromosomes rather than two sets.

Interestingly, less than 3 percent of a person’s DNA contains instructions for building cells; the other 97 percent isn’t active in building anything. Scientists initially called this genetic material “junk DNA,” believing that it didn’t help us in any way and had simply stayed in the gene pool for millions of years. But more recently, scientists have discovered that this genetic information—now called “noncoding DNA”—may be incredibly important in to the evolutionary process. What may be even more surprising is that researchers now believe that as much as a third of our DNA has developed from viruses.

For a long time, the scientific community believed that genetic changes were the product of accidental mutation—errors in copying DNA information from one cell to another that got through our genetic proofreading system. Mutations can also occur when organisms are exposed to radiation or chemicals. Sometimes, a random mutation will give the organism an advantage, which in turn makes its survival and reproduction more likely. This is when natural selection steps in: the mutation increases in successive generations, causing evolution.

More recently, scientists recognized that it would be unlikely for mutations to occur only randomly, because the ability to react to environmental changes and pass on adaptations would be selected for. Additionally, geneticists originally believed that every gene had a single purpose, which would suggest having more than 100,000 genes—but in reality, we only have about 25,000. Thus, genes must interact and shuffle to produce the proteins necessary for human life. Scientists now conceive of genes as “an intricate network of information” that can react to changing circumstances. If one gene fails, another gene can “pick up the slack.” Thus, it is unlikely that small random mutations have led to our evolution, because other genes would simply compensate.

Jean-Baptiste Lamarck, according to popular accounts, was the chief proponent of a theory called inherited acquired traits. The theory holds that traits acquired by a parent during their lifetime could be passed on to their offspring—like giraffes’ necks stretching further and further with each generation to reach leaves on higher branches. According to history, Charles Darwin then proved Lamarck’s theory incorrect with his theory of natural selection. Moalem writes that little of this story is true: Lamarck promoted inherited acquired traits, but he also believed in natural selection—and Darwin believed in both as well. The irony is that the theory of inherited acquired traits isn’t completely wrong.

Barbara McClintock was a revolutionary thinker who was largely ignored by her peers. She received her Ph.D. in 1927 at age 25, and she focused the next 50 years of her career on research on corn genetics. McClintock discovered that in certain circumstances, particularly when the corn was stressed, whole sequences of DNA moved from one place to another and triggered significant changes in the genome. These were often caused by changes in the environment, and the “jumping genes” relocated to certain parts of the genome more often than to other parts. It seemed as though the corn was mutating intentionally rather than randomly.

Barbara McClintock’s findings were largely faced with skepticism until 1983, at age 81, when she received the Nobel Prize. Her discoveries opened the door to the possibility of intentional mutation and much faster evolution. Scientists are still only beginning to understand how these jumping genes (transposons) work—sometimes they copy themselves and insert new material elsewhere, or sometimes they cut themselves out of their starting place and insert somewhere else. One study showed the enormity of the effect they can have: a jumping gene in one line of fruit flies gave them the ability to resist starvation, withstand high temperature, and have a 35 percent longer life expectancy.

McClintock believed that these responses were caused by internal or environmental stress, spurring jumping genes to take a chance on mutating in hopes that they would get a mutation that might help. When that occurs, the proofreading mechanism is suppressed and adaptations are allowed. Today, scientists believe this notion that the genome is not as rigid as once thought, and that mutation is not simply random.

In the 1980s and 1990s, researchers studied other organisms that exhibited the same jumping genes: E. coli, which appeared to target specific areas of its genome where mutations were likely to be advantageous—a process researchers called “hypermutation.” When E. coli was placed in an environment with only lactose (which it could not digest),  studies showed increased mutation in the bacteria’s genome, and not just in an attempt to overcome lactose intolerance.

Moalem transitions to how jumping genes can play into human evolution. In the 19th century, biologist August Weissman divided the body’s cells into two categories: germ cells (egg and sperm cells) and somatic cells (all other kinds of cells). Weissman’s theory, now known as the Weissman barrier, holds that information in somatic cells is never passed on to germ cells. Thus, a mutation in one’s red blood cells would not be passed on to one’s children—only a mutation in the germ line would be passed on. But new research suggests that this might not necessarily the case.

Jumping genes are very active in the early stages of brain development, and Moalem posits that this may help create the variety and individuality that make every brain unique. This activity is only found in the brain because it benefits from individuality—the heart, by contrast, does not. The immune system also welcomes diversity, and scientists from Johns Hopkins have found that jumping genes may help us produce antibodies to develop protection against invaders. However, even if we develop antibodies, we can’t pass them on to our children because of the Weissman barrier. Babies are born with a small number of antibodies, which is why breast milk (which contains some of the mother’s antibodies) is important for babies.

There is now evidence that one-quarter of active (coding) human genes have incorporated DNA from jumping genes. The more we understand about how they work, “the more they may reveal about how our immune systems protect us against disease.” Moalem also notes that as much as half of the “junk DNA” that was previously believed to be unhelpful is actually made up of jumping genes.

Additionally, the jumping genes discovered in human DNA look a lot like virus DNA. A virus is essentially a small portion of genetic code that can’t reproduce on its own—instead, viruses reproduce by infecting a host and using the hosts’ cellular machinery to replicate. Retroviruses are a subset of viruses that are made of RNA (which usually acts as a messenger, copying instructions from DNA to create specific proteins). Retroviruses are able to reverse the process of DNA being copied to RNA, and they can write themselves into a person’s DNA.

Retroviruses can thus write themselves into the DNA of cells in the germ line of an organism, and that organism’s offspring is then born with the virus encoded in  its DNA. If the virus is harmful, it is unlikely that offspring will survive. But if the virus is not harmful, the offspring can survive and reproduce, and the virus becomes a permanent part of the gene pool. Scientists know that at least 8 percent of the human genome is composed of helpful retroviruses. Viruses can help us because they are “master mutators” which can evolve incredibly fast and help us adapt.

Moalem reiterates that jumping genes are probably descended from viruses, and these genes have helped us evolve into complex organisms much faster than we could have otherwise. Humans and African primates also share an interesting genetic trait: our genomes have been modified by a retrovirus in a way that makes it easier for us to be infected by other retroviruses. This capacity to support infection may have enabled us to evolve at a much faster rate, as exposure to other retroviruses could have facilitated more rapid mutation.