A short history of nearly everything - Bill Bryson [208]
It won't have escaped your attention that genes have been commonly implicated in any number of human frailties. Exultant scientists have at various times declared themselves to have found the genes responsible for obesity, schizophrenia, homosexuality, criminality, violence, alcoholism, even shoplifting and homelessness. Perhaps the apogee (or nadir) of this faith in biodeterminism was a study published in the journal Science in 1980 contending that women are genetically inferior at mathematics. In fact, we now know, almost nothing about you is so accommodatingly simple.
This is clearly a pity in one important sense, for if you had individual genes that determined height or propensity to diabetes or to baldness or any other distinguishing trait, then it would be easy—comparatively easy anyway—to isolate and tinker with them. Unfortunately, thirty-five thousand genes functioning independently is not nearly enough to produce the kind of physical complexity that makes a satisfactory human being. Genes clearly therefore must cooperate. A few disorders—hemophilia, Parkinson's disease, Huntington's disease, and cystic fibrosis, for example—are caused by lone dysfunctional genes, but as a rule disruptive genes are weeded out by natural selection long before they can become permanently troublesome to a species or population. For the most part our fate and comfort—and even our eye color—are determined not by individual genes but by complexes of genes working in alliance. That's why it is so hard to work out how it all fits together and why we won't be producing designer babies anytime soon.
In fact, the more we have learned in recent years the more complicated matters have tended to become. Even thinking, it turns out, affects the ways genes work. How fast a man's beard grows, for instance, is partly a function of how much he thinks about sex (because thinking about sex produces a testosterone surge). In the early 1990s, scientists made an even more profound discovery when they found they could knock out supposedly vital genes from embryonic mice, and the mice were not only often born healthy, but sometimes were actually fitter than their brothers and sisters who had not been tampered with. When certain important genes were destroyed, it turned out, others were stepping in to fill the breach. This was excellent news for us as organisms, but not so good for our understanding of how cells work since it introduced an extra layer of complexity to something that we had barely begun to understand anyway.
It is largely because of these complicating factors that cracking the human genome became seen almost at once as only a beginning. The genome, as Eric Lander of MIT has put it, is like a parts list for the human body: it tells us what we are made of, but says nothing about how we work. What's needed now is the operating manual—instructions for how to make it go. We are not close to that point yet.
So now the quest is to crack the human proteome—a concept so novel that the term proteome didn't even exist a decade ago. The proteome is the library of information that creates proteins. “Unfortunately,” observed Scientific American in the spring of 2002, “the proteome is much more complicated than the genome.”
That's putting it mildly. Proteins, you will remember, are the workhorses of all living systems; as many as a hundred million of them may be busy in any cell at any moment. That's a lot of activity to try to figure out. Worse, proteins' behavior and functions are based not simply on their chemistry, as with genes, but also on their shapes. To function, a protein must not only have the necessary chemical components, properly assembled, but then must also be folded into an extremely specific shape. “Folding” is the term that's used, but it's a misleading