Some of us will be able to add that most DNA isn't in the form of genes, but is just `junk' left over from some distant part of our evolutionary history. The junk gets a free ride on the reproductive roller-coaster, and it survives because it is `selfish' and doesn't care what happens to anything except itself.
Here ends the folk view of evolution. We've parodied it a little, but not by as much as you might hope. The first part is a lie-to-children about natural selection; the second part is uncomfortably close to `neo-Darwinism', which for most of the past 50 years has been the accepted intellectual heir to The Origin. Darwin told us what happens in evolution; neo-Darwinism tells us how it happens, and how it happens is DNA.
There's no question that DNA is central to life on Earth. But virtually every month, new discoveries are being made that profoundly change our view of evolution, genetics, and the growth and diversification of living creatures. This is a vast topic, and the best we can do here is to show you a few significant discoveries and explain why they are significant.
Just as physics replaced Newton by Einstein, there has been a major revolution in the basic tenets of biology, so we now have a different, more universal view of what drives evolution. The `folk' evolutionary viewpoint: `I've got this new mutation. I have become a new kind of creature. Is it going to do me any good?' is not the way modern biologists think.
There are many things wrong with our folk-evolution story. In fact we've deliberately constructed it so that every single detail is wrong. However, it's not very different from many accounts in popular science books and television programmes. It assumes that primitive animals alive today are our ancestors, when they are our cousins. It assumes that we `came from' apes, when of course the ape-like ancestor of man is the same creature as the man-like ancestor of modem apes. More seriously, it assumes that mutations in the genetic material, the changes that natural selection has to work on - indeed, to select among - are checked out as soon as they appear, and labelled `bad' (the organism dies, or at least fails to breed) or `good' (the animal contributes its progeny to the future).
Until the early 1960s, that was what most biologists thought too. Indeed, two very famous biologists, J.B.S. Haldane and Sir Ronald Fisher, produced important papers in the mid-1950s espousing just that view. In a population of about 1000 organisms, they believed, only about a third of the breeding population could be `lost' to bad gene variants, or could be ousted by organisms carrying better versions, without the population moving towards extinction. They calculated that only about ten genes could have variants (known as `alleles') that were increasing or decreasing as proportions of the population. Perhaps twenty genes might be changing in this way if they were not very different in `fitness' from the regular alleles. This picture of the population implied that almost all organisms in a given species must have pretty much the same genetic make-up, except for a few which carried the good alleles coming in, and winning, or the bad alleles on the way out. [1] These exceptions were mutants, famously and stupidly portrayed in many SF films.
However, in the early 1960s Richard Lewontin's group exploited a new way to investigate the genetics of wild (or indeed any) organisms. They looked at how many versions of common proteins they could find in the blood, or in cell extracts. If there was just one version, the organism had received the same allele from both of its parents: the technical term here is `homozygous'. If there were two versions, it had received different ones from each parent, and so was `heterozygous'.
What they found was totally incompatible with the Fisher-Haldane picture.
They found, and this has been amply confirmed in thousands of wild populations since, that in most organisms, about ten percent of
[1] They made exceptions for manifestly `unimportant' but very diverse sets of alleles like blood groups, but in those cases it didn't seem to matter much which kind you had.
genes are heterozygous. We now know, thanks to the Human Genome Project, that human beings have about 34,000 genes. So about 3400 are heterozygous, in any individual, instead of the ten or so predicted by Haldane and Fisher.
Furthermore, if many different organisms are sampled, it turns out that about one-third of all genes have variant alleles. Some are rare, but many of them occur in more than one per cent of the population.
There is no way that this real-world picture of the genetic structure of populations can be reconciled with the classical view of population genetics. Nearly all current natural selection must be discriminating between different combinations of ancient mutations. It's not a matter of a new mutation arriving and the result being immediately subjected to selection: instead, that mutation must typically hang around, for millions of years, until eventually it ends up playing a role that makes enough of a difference for natural selection to notice, and react.
With hindsight, it is now obvious that all currently existing breeds of dog must have been 'available'- in the sense that the necessary alleles already existed, somewhere in the population - in the original domesticated wolves. There simply hasn't been time to accumulate the necessary mutations purely in modern dogs. Darwin knew about the amount of cryptic and overt variation in pigeons, too. But his successors, hot on the trail of the molecular basis of life, forgot about wolves and pigeons. They pretty much forgot about cells. DNA was complicated enough: cell biology was impossible, and as for understanding an organum ...
Lewontin's discovery was a significant turning point in our understanding of heredity and evolution. It was at least as radical as the much better publicised revolution that replaced Newton's physics with Einstein's, and it was arguably more important. We will see that in the last year or so there has been another, even more radical, revision of our thinking about the control of cell biology and development by the genes. The whole dogma about DNA, messenger RNA, and proteins has been given a reality check, and science's internal `auditors' have rendered it as archaic as Fisher's population genetics.
It is commonly assumed - not only by the average television producer of pop science half-hours, but also by most popular science book authors - that now we know about DNA, the `secret of life', evolution and its mechanisms are an open book. Soon after the discovery of DNA's structure and mechanism of replication by James Watson and Francis Crick, in the late 1950s, the media - and biology textbooks at all levels - were beginning to refer to it as the `Blueprint for Life'. Many books, culminating with Dawkins's The Selfish Gene in the 1970s, promoted the view that by knowing about the mechanism of heredity, we had found the key to all of the important puzzles of biology and medicine, especially evolution.
There was soon to be a major tragedy, resulting from a medical application of that mistaken view. The sedative thalidomide was increasingly being prescribed, and bought over the counter, to treat nausea and other minor discomforts of the early weeks of pregnancy.
Only later was it discovered that in a small proportion of cases, thalidomide could cause a type of birth defect known as phocomelia, in which arms and legs are replaced by partially developed versions that resemble a seal's flippers.
It took a while for anyone to notice, partly because few general practitioners had experience of phocomelia before 1957. In fact, very few of them had ever seen a case at all, but after 1957 they began to see two or three in a year. A second reason was that it was very difficult to tie this defect to a particular potion or treatment: pregnant women famously take a great variety of dietary additives, and often they don't remember precisely what they've taken. Nevertheless, by 1961 some medical detective work had tied the spate of phocomelia down to thalidomide.