Lewis Wolpert
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Genes control development of every bit of our bodies by determining which proteins are present in our cells, but I have little sympathy with those who talk about genes for this or that, such as good looks or intolerance. Whether or not such characteristics have a genetic basis is a tough problem. The language is misleading. There is no gene, for example, for the eye; many hundreds, if not thousands, are involved in its development, and a fault in just one can lead to major abnormalities.
The language in which many of the effects of genes is described leads to confusion. No sensible person would say that the brakes of a car are for causing accidents. Yet, using a convenient shorthand, there are numerous references to, for example, the gene for criminality. When the brakes of the car, which are there for safe driving, fail, then there is an accident. Similarly, if criminality has some genetic basis, which is by no means certain, then it is not because there is “a gene” for criminality but because alterations in many genes have resulted in this undesirable effect. Such alterations could have affected how the brain developed or could cause changes in the way the nerve cells of the adult brain function.
It is important to realise that, at present, knowing all the genes of an individual will not tell us how the cells function or how the embryo develops. Consider this set of words: “alters impediment marriage me of not not or to true is minds with love love which let it alteration the finds bends remover remove admit when the to”. Taken from a sonnet by Shakespeare, these words suggest the subject matter of the poem - it seems to be about love and marriage - but give no idea whatsoever of the ideas expressed. This is the position we are in in relation to the human genome. We know the whole DNA sequence of the human genome - that is, the DNA sequence of all human genes - and it is a tremendous achievement to have sequenced all that DNA, because by it we are able to identify each of the 30,000 or so genes that control our development and our lives. But each of those genes is like a word in the poem, and by itself tells us little about how the protein it codes for will act in the body or how it will interact with other proteins. Knowing the human genome sequence is only the beginning, and there is an enormous amount that it cannot tell us. We need to know how it controls the development of the embryo; then we would know how the sonnet reads:
Let me not to the marriage of true minds
Admit impediment. Love is not love
Which alters when it alteration finds
Or bends with the remover to remove
Just six years ago, two versions of the human genome sequence were published. Both versions are composite sequences derived from the genomes of many anonymous donors. But now one of the principals behind this work, the scientist Craig Venter, has sequenced his own genome. No one expects to understand what makes Venter tick by looking at his genome, but there are some potentially useful things one can find out from a genome sequence, such as looking for known mutations that increase the risk of various diseases.
Will it not be possible to work out from the genome just how the whole will function? Not at present, any more than we can reconstruct the sonnet from its words. The key to understanding living systems is proteins, and genes merely provide the information for making proteins. Knowing the human genome will tell us what proteins cells can make, because the coding regions can be identified, but it will not easily tell us when or where they will be made in the developing embryo. This depends on the control regions of genes, which cannot be identified in the genome without much more research. In addition, there will be proteins whose function is still unknown.
The future will be research into determining what the sequence of nucleotides tells us about cell behaviour and the complex interactions in the cells, from DNA to proteins. And what the proteins do.
How We Live and Why We Die: The Secret Lives of Cells by Lewis Wolpert (Faber & Faber)
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