A short history of nearly everything

The outcome of all this was that in January 1953, Wilkins showed Watson Franklin’s images, “apparently without her knowledge or consent.” It would be an understatement to call it a significant help. Years later Watson conceded that it “was the key event . . . it mobilized us.” Armed with the knowledge of the DNA molecule’s basic shape and some important elements of its dimensions, Watson and Crick redoubled their efforts. Everything now seemed to go their way. At one point Pauling was en route to a conference in England at which he would in all likelihood have met with Wilkins and learned enough to correct the misconceptions that had put him on the wrong line of inquiry, but this was the McCarthy era and Pauling found himself detained at Idlewild Airport in New York, his passport confiscated, on the grounds that he was too liberal of temperament to be allowed to travel abroad. Crick and Watson also had the no less convenient good fortune that Pauling’s son was working at the Cavendish and innocently kept them abreast of any news of developments and setbacks at home.

Still facing the possibility of being trumped at any moment, Watson and Crick applied themselves feverishly to the problem. It was known that DNA had four chemical components-called adenine, guanine, cytosine, and thiamine-and that these paired up in particular ways. By playing with pieces of cardboard cut into the shapes of molecules, Watson and Crick were able to work out how the pieces fit together. From this they made a Meccano- like model-perhaps the most famous in modern science-consisting of metal plates bolted together in a spiral, and invited Wilkins, Franklin, and the rest of the world to have a look. Any informed person could see at once that they had solved the problem. It was without question a brilliant piece of detective work, with or without the boost of Franklin’s picture.

The April 25, 1953, edition of Nature carried a 900-word article by Watson and Crick titled “A Structure for Deoxyribose Nucleic Acid.” Accompanying it were separate articles by Wilkins and Franklin. It was an eventful time in the world-Edmund Hillary was just about to clamber to the top of Everest while Elizabeth II was imminently to be crowned queen of England-so the discovery of the secret of life was mostly overlooked. It received a small mention in the News Chronicle and was ignored elsewhere.

Rosalind Franklin did not share in the Nobel Prize. She died of ovarian cancer at the age of just thirty- seven in 1958, four years before the award was granted. Nobel Prizes are not awarded posthumously. The cancer almost certainly arose as a result of chronic overexposure to X-rays through her work and needn’t have happened. In her much-praised 2002 biography of Franklin, Brenda Maddox noted that Franklin rarely wore a lead apron and often stepped carelessly in front of a beam. Oswald Avery never won a Nobel Prize either and was also largely overlooked by posterity, though he did at least have the satisfaction of living just long enough to see his findings vindicated. He died in 1955.

Watson and Crick’s discovery wasn’t actually confirmed until the 1980s. As Crick said in one of his books: “It took over twenty-five years for our model of DNA to go from being only rather plausible, to being very plausible . . . and from there to being virtually certainly correct.”

Even so, with the structure of DNA understood progress in genetics was swift, and by 1968 the journal Science could run an article titled “That Was the Molecular Biology That Was,” suggesting-it hardly seems possible, but it is so-that the work of genetics was nearly at an end.

In fact, of course, it was only just beginning. Even now there is a great deal about DNA that we scarcely understand, not least why so much of it doesn’t actually seem to do anything. Ninety- seven percent of your DNA consists of nothing but long stretches of meaningless garble-“junk,” or “non-coding DNA,” as biochemists prefer to put it. Only here and there along each strand do you find sections that control and organize vital functions. These are the curious and long-elusive genes.

Genes are nothing more (nor less) than instructions to make proteins. This they do with a certain dull fidelity. In this sense, they are rather like the keys of a piano, each playing a single note and nothing else, which is obviously a trifle monotonous. But combine the genes, as you would combine piano keys, and you can create chords and melodies of infinite variety. Put all these genes together, and you have (to continue the metaphor) the great symphony of existence known as the human genome.

An alternative and more common way to regard the genome is as a kind of instruction manual for the body. Viewed this way, the chromosomes can be imagined as the book’s chapters and the genes as individual instructions for making proteins. The words in which the instructions are written are called codons, and the letters are known as bases. The bases-the letters of the genetic alphabet-consist of the four nucleotides mentioned a page or two back: adenine, thiamine, guanine, and cytosine. Despite the importance of what they do, these substances are not made of anything exotic. Guanine, for instance, is the same stuff that abounds in, and gives its name to, guano.

The shape of a DNA molecule, as everyone knows, is rather like a spiral staircase or twisted rope ladder: the famous double helix. The uprights of this structure are made of a type of sugar called deoxyribose, and the whole of the helix is a nucleic acid-hence the name “deoxyribonucleic acid.” The rungs (or steps) are formed by two bases joining across the space between, and they can combine in only two ways: guanine is always paired with cytosine and thiamine always with adenine. The order in which these letters appear as you move up or down the ladder constitutes the DNA code; logging it has been the job of the Human Genome Project.

Now the particular brilliance of DNA lies in its manner of replication. When it is time to produce a new DNA molecule, the two strands part down the middle, like the zipper on a jacket, and each half goes off to form a new partnership. Because each nucleotide along a strand pairs up with a specific other nucleotide, each strand serves as a template for the creation of a new matching strand. If you possessed just one strand of your own DNA, you could easily enough reconstruct the matching side by working out the necessary partnerships: if the topmost rung on one strand was made of guanine, then you would know that the topmost rung on the matching strand must be cytosine. Work your way down the ladder through all the nucleotide pairings, and eventually you would have the code for a new molecule. That is just what happens in nature, except that nature does it really quickly-in only a matter of seconds, which is quite a feat.

Most of the time our DNA replicates with dutiful accuracy, but just occasionally-about one time in a million-a letter gets into the wrong place. This is known as a single nucleotide polymorphism, or SNP, familiarly known to biochemists as a “Snip.” Generally these Snips are buried in stretches of noncoding DNA and have no detectable consequence for the body. But occasionally they make a difference. They might leave you predisposed to some disease, but equally they might confer some slight advantage-more protective pigmentation, for instance, or increased production of red blood cells for someone living at altitude. Over time, these slight modifications accumulate in both individuals and in populations, contributing to the distinctiveness of both.

The balance between accuracy and errors in replication is a fine one. Too many errors and the organism can’t function, but too few and it sacrifices adaptability. A similar balance must exist between stability in an organism and innovation. An increase in red blood cells can help a person or group living at high elevations to move and breathe more easily because more red cells can carry more oxygen. But additional red cells also thicken the blood. Add too many, and “it’s like pumping oil,” in the words of Temple University anthropologist Charles Weitz. That’s hard on the heart. Thus those designed to live at high altitude get increased breathing efficiency, but pay for it with higher-risk hearts. By such means does Darwinian natural selection look after us. It also helps to explain why we are all so similar. Evolution simply won’t let you become too different-not without becoming a new species anyway.

The 0.1 percent difference between your genes and mine is accounted for by our Snips. Now if you compared your DNA with a third person’s, there would also be 99.9 percent correspondence, but the Snips would, for the most part, be in different places. Add more people to the comparison and you will get yet more Snips in yet more places. For every one of your 3.2 billion bases, somewhere on the planet there will be a person, or group of persons, with different coding in that position. So not only is it wrong to refer to “the” human genome, but in a sense we don’t even have “a” human genome. We have six billion of them. We are all 99.9 percent the same, but equally, in the words of the biochemist David Cox, “you could say all humans share nothing, and that would be correct, too.”

But we have still to explain why so little of that DNA has any discernible purpose. It starts to get a little unnerving, but it does really seem that the purpose of life is to perpetuate DNA. The 97 percent of our DNA commonly called junk is largely made up of clumps of letters that, in Ridley’s words, “exist for the pure and simple reason that they are good at getting themselves duplicated.”[45] Most of your DNA, in other words, is not devoted to you but to itself: you are a machine for reproducing it, not it for