Feb 2 JDN 2460709

In the last post I said I’d explain the basics of evolution, then went into a bunch of detail about genetics. Why all this stuff about DNA? Weren’t we supposed to be talking about evolution? Yes—but it’s impossible to truly understand evolution without understanding DNA. This unity between genetics and evolution is called the Modern Synthesis, and it is the unified field theory of the life sciences. It’s quite different from what Darwin invented in 1859, but the fundamental insights were his; the Modern Synthesis is a body of flesh over the skeleton of Darwinian evolution. Now that I have explained the basics of DNA, it is time to discuss evolution itself.

The fundamental unit of evolution is the gene. (Darwin, among others, insisted that the fundamental unit of evolution is the organism, because it is organisms that are born and die. There is some truth to this, but given the presence of phenomena like kin selection and genetic drift, we also need to consider genes themselves. Richard Dawkins makes a distinction between “replicators” (genes) and “vehicles” (organisms) that makes a great deal of sense to me—both are necessary parts of the same system, and it’s a little silly to ask which is “more fundamental”.) The fundamental unit of evolution is not the population or the species; it is populations that evolve, but they evolve by natural selection acting upon individuals and genes. Natural selection is not sensitive to “the good of the species”; it is only sensitive to the good of the organism and the good of the gene.

A gene is a section of DNA that, when processed by the appropriate proteins, produces a particular protein. Most DNA is not in the form of genes. The majority of DNA has no effect—you can change it without affecting the organism—and most of the rest is involved in regulating the genes, not in producing proteins. Yet, genes are the recipes by which we are made. Human beings have genes for hemoglobin that oxygenates our blood, genes for melanin that pigments our skin, genes for serotonin that transmits signals in our brains, genes for keratin that makes up our hair, and about 46,000 other genes that produce other proteins (the Human Genome Project is still working on the exact number). An allele is a particular variant of a gene which produces a particular variant of the resulting protein. Alleles in melanin genes give different people different colors of skin; a particular allele in a hemoglobin gene gives some people sickle-cell anaemia.

When the distribution of alleles in a population changes, that is evolution. Yes, that’s all “evolution” means: Changes of distribution in alleles in a population. When a baby is born, that’s evolution. When a person dies, that’s evolution. This is what we mean when we say that evolution is a fact; it is a fact that alleles do change distribution in populations. Individuals do not evolve, populations evolve. You will never see a dog turn into a cat, nor an ape to a human. You could see, if you were watching for millions of years, a population of animals that started very dog-like and got increasingly cat-like with each generation, or a population of animals that started very ape-like and got increasingly human-like with each generation. Even these latter are not necessary occurrences; under different environmental circumstances, the same genes can evolve in completely different directions.

Fitness is the expected number of copies that an allele is likely to produce in the next generation.(There are a few subtly different ways of defining fitness; the one I prefer is the expected value of the number of copies of a given allele in the next generation. The fitness f of an allele a at generation t is given by the expectation of the number n of copies of that allele in that population at generation t+1: f(a,t) = E[n(a,t+1)]This is an \inclusive fitness measure, which accounts for kin selection better than exclusive fitness measures like “predicted grandchildren” or “expected number of reproductively-viable offspring”. In practical terms these generally give the same results; but when they don’t, the inclusive measure is to be preferred.)

Fitness is a probabilistic notion—alleles with high fitness are likely to be passed on, but this is not guaranteed. “Survival of the fittest” ultimately just means that genes that are likely to make many copies are likely to have many copies. It has been said that this is a tautology, and indeed it is; but so is the Pythagorean Theorem. Some tautologies are useful, and all tautologies are undeniably true.

What causes evolution? Organisms are born, reproduce, and die. Any time this happens, it changes the distribution of alleles in the population—it is evolution. If there was a reason why the ones who lived lived and the ones who died died, then the actual number of copies of each allele in the population will reflect the fitness of those alleles; this is called natural selection. On the other hand, if it just happened by chance, then the distribution of alleles won’t match the fitness; this is called genetic drift. Examples of each: Trees are tall, giraffes eat leaves, so giraffes with longer necks get more food and live longer—that’s natural selection. A flood rips through the savannah and kills half of the giraffes, and it just happens that more long-necked than short-necked giraffes die—that’s genetic drift. The difference can be subtle, since sometimes we don’t know what the reasons are; if it turned out that there was some reason why floods are more likely to kill long-necked giraffes (they can’t swim as well?), then in fact what we thought was genetic drift was really natural selection. But notice: Natural selection is not chance. Natural selection is the opposite of chance. If evolution happens by chance, that’s genetic drift. Natural selection is evolution that happens for a reason.

Natural selection changes populations, but what causes them to separate into distinct species? Well, a species is really a breeding population—it is a group of organisms that regularly interbreeds within the group and does not regularly interbreed outside the group. In most cases, breeding between species is actually impossible; but in many cases it is simply rare. Indeed, there is a particularly interesting case called a ring species, in which interbreeding possibilities rest on a continuum rather than being sharply delineated. In a ring species, there are several distinct populations for which some can interbreed easily, others can interbreed with difficulty, and others can’t inbreed at all. A classic case is the Ensatina salamanders who live in the Central Valley in California. There are nineteen populations, and each can interbreed with its adjacent populations—but the two populations at the far ends cannot interbreed. Ensatina eschscholtzii eschscholtzii can interbreed with E.e. croceater, which can interbreed with E.e. oregonensis, and so on all the way to E.e. klauberi—but E.e. eschscholzii on one end can’t interbreed with E.e. klauberi on the other end. Are they different “species”? It’s difficult to say. If all the intermediates died out, we would call them different species, Ensatina escholzii and Ensatina klauberi; but in fact genes do sometimes pass between them, because they can both interbreed with the intermediates. Really, the concept “species” fails to capture the true complexity of the situation.

This is not a problem for evolutionary theory—it is a prediction of evolutionary theory. We should expect to see new species occasionally forming, and while they are in the process of forming there should be many intermediates that aren’t yet distinct species. Evolution predicts gradual divergence, and sometimes we are lucky enough to see that divergence in process.

Natural selection can only act upon alleles that already exist; it chooses the best out of what’s available, not the best that could possibly exist. This is why dolphins breathe air instead of water; breathing water would be much better for their lifestyle, but no dolphin has yet been born who can breathe water. The alleles aren’t there, so natural selection cannot act upon them. If a mutant dolphin is someday born who can breathe water, as long as they don’t suffer from other problems as a result of their mutation, they are likely to live a long time and have lots of offspring; in a hundred generations perhaps water-breathing dolphins would form a new species, or even replace air-breathing dolphins. And notice how short a time that is: 100 generations of dolphins is only about 1000 years. We could watch this happening in historical time. If it had happened a million years ago, the fossil record would probably never show the intermediate forms. This is why we don’t see transitional forms between closely-related species; because the differences are so subtle, the necessary changes can occur very rapidly, in too few generations to ensure fossilization.

Indeed, monogenic traits—those that can be changed by a single mutation—never produce transitional forms. There is a single gene for sickle-cell anaemia in humans; we should not expect to see people with “30\% sickle-cell anaemia”, because there are only three options: you either have no copies of the sickle-cell allele (normal), you have one copy (sickle-cell trait), or you have two copies (sickle-cell anaemia). In fact, in this particular case, the one-copy variant isn’t even mild anaemia; it is a generally healthy non-anaemic state that offers protection against malaria. There is a single gene for six fingers in humans. Two copies gives you six fingers; one copy doesn’t do anything. Even if we had access to every individual organism that ever lived, we still wouldn’t see transitional forms for monogenic traits. Given that we actually have fossils of less than one in ten billion organisms that ever lived, it’s not surprising that most evolutionary changes leave no mark in the fossil record.

Furthermore, it’s important to understand that natural selection, even when there is plenty of variation to act on, does not produce perfectly-adapted organisms. It only produces organisms that are good enough to survive and pass on their alleles. In fact, there can be multiple fit alleles of the same gene in a population—all different, perhaps even some better than others, but each good enough to keep on surviving.

Indeed, the fitness of one allele can increase the fitness of another allele, in a number of different ways. The most morally-relevant ones only make sense in terms of game theory, so I will wait until later posts to get into them, but there are a few worth mentioning here. The first is co-evolution. Organisms evolve to suit their environments—but part of an organism’s environment consists of other organisms. Bees would not function if there were no flowers—but nor would flowers function without bees. So which came first, the bee or the flower? Neither. Ancient ancestors of each evolved together, co-evolved, the proto-flowers growing more flower-like as the proto-bees grew more bee-like, until finally an equilibrium was reached at the bees and flowers we see today.

Another way that organisms can affect the evolution of other organisms is through frequency-dependent selection, in which the fitness of a given allele depends upon the distribution of other alleles of the same gene. The most important case of frequency-dependent selection is in sex dimorphism, the differences between sexes within a species. If there are more males than females, the fitness of females goes up—it pays to be female; you’ll get your choice of males. Conversely, if there are more females than males, it pays to be male. Hence, over time, sex distributions reach an equilibrium at 50% male and 50% female, which has happened in almost every species (eusocial insects are the only major exception, and it’s due to their weird genetics). There are other cases of frequency-dependent selection as well; for instance, in stag beetles (Lucanidae), there are three kinds of males, called “alpha”, “beta”, and “gamma”. Alpha males have large horns and fight heavily with other alpha males; they risk being killed in the process, but if they win the fight, they get all the best females. Beta males have short horns and only fight other beta males; this limits their mating pool, but prevents them from being killed by alpha males. Finally, gamma males look just like females and will occasionally sneak past an alpha male and mate with his females. This is frequency-dependent selection because the success of each strategy depends on the other strategies in a fashion similar to rock-paper-scissors. If gamma males become very common, beta males will become more successful, because they won’t get cheated the way alpha males do. If beta males become common, alpha males will become more successful, because they can beat beta males in fights. If alpha males become common, gamma males will become more successful, because they can cheat alpha males. In the long run, the system settles into an equilibrium with a certain fraction of all three types.

A third way alleles affect other alleles is in sexual selection; in sexual selection, the alleles of one sex affect the alleles of the other sex, because sexual compatibility has obvious advantages. For instance, when there are lots of alleles in peahens that make them attracted to big, colorful tails, there is a fitness advantage to being a peacock with a big, colorful tail. Hence, alleles for big, colorful tails in peacocks will be selected. But then, if all the males have big, colorful tails, there is a fitness advantage to being a female who prefers big, colorful tails, and so a positive feedback loop forms; the end result is peacocks with ridiculously huge, ridiculously colorful tails and peahens who love them for it.

Everything above is very technical and scientific, and I imagine it is not very controversial or offensive to anyone. In future posts, I’ll get into the stuff that really upsets people, the true source of controversy on evolution.