The Evolutionary Psychology FAQ

Edward H. Hagen, Institute for Theoretical Biology, Berlin

Why are genes selfish?

Richard Dawkins wrote a very popular book called the Selfish Gene that explained, for a popular audience, many of the exciting new theories and discoveries being made in evolutionary biology in the 1960’s and 70’s. The metaphor Dawkins chose, the selfish gene, was an extremely powerful metaphor, so powerful that it has often overshadowed the science itself! The controversies that swirl around EP are often tightly bound up with Dawkins’ metaphor. If our genes are selfish, are we all, deep down, unalterably selfish ourselves? Why did Dawkins chose this metaphor, what does it really mean, and what are its implications for EP and human nature?

Simplifying greatly for the sake of the argument, there is a molecule, called a nucleotide, that comes in four different types, A, C, G, & T. Large numbers of these nucleotides can be linked together in a linear strand to make a much bigger molecule called DNA. Schematically, DNA looks like this: ACGTGCCT…etc. Human DNA consists of about 3 billion nucleotides chained together. Simplifying greatly again, small sections of the DNA strand called ‘genes’, which are usually several hundred to several thousand nucleotides long, are able to create a different type of long, linear molecule called a protein. Proteins are a kind of plastic—technically, a polymer—that, like the DNA chain, are made up of a small number of different molecular building blocks called amino acids (there are 20 different amino acid building blocks ). Just as the different chemical structure of the plastic in a plastic bag versus the chemical structure of the plastic in dental floss versus the chemical structure of the plastic in bullet-proof vests gives these different materials very different properties, the exact sequence of the different amino acids in a particular protein determines its biological properties. Different amino acid sequences give different proteins very different properties.

To summarize, the sequence of nucleotides in small sections of our DNA (called genes) determines the sequence of amino acids of proteins created by the genes, and these amino acid sequences determine the proteins’ biological properties. Although scientists are still debating the exact number, DNA contains somewhere between 30,000 and 60,000 different genes, and can therefore create between 30,000 and 60,000 different proteins, each with unique properties. As I mentioned, proteins are a kind of plastic, so our DNA functions, in part, to create a large number of different plastics with different properties. These highly specialized plastics with very special biological properties are what our bodies are made of. DNA is a kind of lumber yard that provides, among other things, a large number of plastic building materials for making organisms.

Simplifying once more (this time by ignoring sex), individuals pass on an exact copy of their DNA chain to their offspring: if my body is made up of a particular set of plastics, because my offspring has an exact copy of my DNA, my offspring’s body will be make up of exactly the same set of plastics, and so it will be exactly like me. Occasionally, however, one of the molecules in the DNA chain (i.e., one of the A, C, G, or T nucleotides), can become mutated (altered) by cosmic radiation, environmental toxins, etc.; these mutagens turn one type of nucleotide into another type of nucleotide (e.g., an A turns into G). If I pass on this mutated DNA, where only one of the 3 billion nucleotides is different from my own, then my offspring will be made of proteins that are almost exactly like mine, except for the protein which was made by the mutated section of DNA (the mutated gene), which will be a different protein with different properties. My offspring will not be exactly like me—he will be said to have a different phenotype (body type).

Imagine that the gene that was mutated was the gene that made the plastic forming the lens of the eye. This plastic has a very special property: it is almost completely transparent. Most proteins, like those forming your skin, muscles, hair, etc., are not transparent. Because my offspring has a mutated form of the lens gene, there are now two types of genes in the population that make the lens protein: the normal version, possessed by most individuals (which I will call Tnormal, for normal transparency) and the mutated version possessed by my offspring. Different forms of the same gene are called alleles. Because it is far easier to make something worse than it is to make it better, most of the time when the gene producing the lens protein is mutated (and this happens very rarely), the altered lens protein produced by the mutated gene will not be as transparent as the original version (so I will label this allele Tlow, for low transparency). My offspring will therefore not be able to see as well as other members of his species who have the Tnormal allele, and thus normal versions of the lens protein.

Let’s assume that my offspring’s lens protein is only slightly less transparent than the normal version. He will be able to live his life and have offspring. The population will therefore contain a mix of lens alleles; most of the population will have Tnormal, but some will have Tlow. Because those with the Tlow allele will not be able to see quite as well as other members of their species possessing Tnormal, on average they will not have as many offspring. Perhaps they notice prey slightly less often, and thus not have quite as much food, or perhaps they fail to notice predators slightly more often, and will therefore be killed and eaten at a slightly higher frequency. Over many, many generations, the fraction of individuals with the Tlow allele will decrease relative to those with the Tnormal allele simply because individuals possessing the Tlow allele produce, on average, fewer offspring. We say that the Tlow allele producing the less transparent lens protein is selected against, and that the frequency of this allele decreases with time. Notice that, if the total population size remains constant, that the decrease in frequency of the Tlow allele results in an increase in the frequency of the Tnormal allele.

Imagine another mutation of the normal lens allele, creating a third allele (Tsuper) that produces a super transparent lens protein. The population now contains three alleles, Tlow, Tnormal, and Tsuper. Individuals possessing the Tsuper allele detect prey, on average, at slightly higher frequencies, and thus have more food, and they more frequently detect predators and therefore are eaten slightly less frequently. As a consequence, on average, they have more offspring than individuals possessing Tnormal. Over many, many generations, the frequency of the Tsuper allele will increase in the population, whereas the frequencies of the Tnormal and Tlow alleles will decrease, and perhaps disappear altogether. This is called evolution by natural selection: the frequencies of the three alleles have changed as a consequence of their reproductive effects. Over time, a population will acquire alleles that produce proteins that better solve critical reproductive problems, and lose alleles that produce proteins that less effectively solve these problems. There is widespread agreement that evolution by natural selection is responsible for the origins of the sophisticated organs and tissues like hearts, lung, livers, etc., that enable organisms to reproduce.

Because, in a population of a given size, the increase in the frequency of Tsuper must decrease the frequencies of the other alleles, biologists began saying that different alleles were ‘competing’. (Usually, but not always, alleles increase their frequency by causing individuals possessing them to produce, on average, more offspring.) Dawkins, highlighting the iron-clad logic that alleles increase their frequency in the population if they cause more copies of themselves to be made relative to other alleles, and that by increasing their own frequency, they decrease the frequency of the alternative (competing) alleles, termed genes ‘selfish’. Alleles increase their frequency at the expense of other alleles.

Copyright 1999-2002 Edward H. Hagen