The clone by clone approach — tearing out pages of the map, sequencing each one and ordering them by looking at the overlaps — revealed about a thousand segments of DNA that looked us if they might code tor a protein. Seven hundred or so are identical to genes already found within ourselves or elsewhere and m;iy represent iiselul bits of DNA. Many, no doubt, cause diseases when (hey go wrong. Some may be impostors; segments that make nothing but have, by chance, an identity that resembles that of a productive section of the genome. Even this, the smallest chromosome, has no shortage of genes. The smallest is a mere thousand bases long, its largest more than five hundred times bigger. Some are uninterrupted, but most are fractured by many inserted sequences of non-coding DNA. To make matters even more complicated, two genes appear within the structure of others. They are genes within genes; read (like a Hebrew sentence in an English book) not from left to right but from right to left.

Most of the remainder of the chromosome is a story of waste and decay. It hides within itself eight or so lengthy duplications, in which whole segments of the instructions are, for some reason, doubled up. The wrecks of genes are everywhere, and about a fifth of the sequences that might once have made something are present only as pseudogenes. Most of the actual workers are — just like the producers of the red blood pigment — members of gene families; and most of those families are filled with genetic black sheep, pseudogenes, who rest on their laurels while their kin go about their business. Some of its genes are responsible for proteins associated with the immune system. They work together as a family of dozens of productive members, but are accompanied by twice as many decayed relatives with a home nearby.

Thirty or so disorders — from cancers to errors in foetal development to a tendency towards schizophrenia — have now been uncovered on this short chromosome: a small part of the thousands that inflict the human race, but a hint of the huge numbers of ways that DN A can go wrong. Most of the proteins mapped to chromosome 22 have no known function. What some do can be guessed at by comparing them with others from elsewhere in the human genome, or from the rest ol life, but the majority are anonymous factories, hard at work but with, as yet, no hint about what they made.

Other chromosomes have the same general nature as does the smallest, although each has its quirks. The next in line, chromosome 21, has a personality of its own. Already famous as the sources of the commonest human inborn abnormality, Down's syndrome (present in about one in seven hundred live births) and as the site of one of the genes predisposing to Alzheimer's disease, this structure has some thirty-three million base pairs — about one per cent of the total. One end is stuffed with copies of the same sequence, multiplied again and again; but the other has the machinery. Not, however, very much; for chromosome 21, although about the same size as number 2.2, has only half its number of genes.

Its two hundred and twenty-five working segments (nine-tenths of which were new to science) seem a modest endowment. Perhaps its depauperised state explains why chromosome 21 is the only chromosome (apart from the sex chromosomes) which the body can tolerate in extra copy. Children with Down's syndrome suffer from fifty or more distinct problems, ranging from heart disease and a tendency to leukemia to difficulties in breathing. One severe problem is their premature ageing and memory loss. That symptom resembles those of Alzheimer's disease — and one of the genes responsible for the early-onset form of that illness is found in chromosome 2.1. Perhaps some of the chromosome's other genes will turn out to be associated with other ailments common to Down's children.

Its other genes include those reponsible for two forms of inborn deafness and for amyotrophic lateral sclerosis: a condition known in the United States as Lou Gehrig's Disease after the New York Yankee shiver who died of the illness, but in Britain indissoluhly linked 10 ilu- ^reat physicist Stephen Hawking. Those with the condition suffer from a loss of nerve cells in the brain *** spinal cord and, as a result, slowly lose all power of movement. The problem lies with an enzyme whose job is to clean up wastes inside the cell: when it fails, the nerves are slowly poisoned.

Chromosome 2.1 may look like a run-down industrial estate with few of its windows lit up; but at the other extreme of economic activity, chromosome 6 is full of active genes. It is in the forefront of the body's genetic defences. One section has long been known to be responsible for much of the body's immune defences. The crucial segment is only about a tenth the size of chromosome 2.1, but contains well over a hundred genes (as well as a respectable number of relics that have given up the functional ghost). Many share a certain identity and have arisen by duplication from ancient ancestral genes. Much of their job involves binding to the proteins of an invader and passing on information as to its identity to the white blood cells that then swing into attack. Others code for statements of individual entity on the cell surface.

Because so many genes are involved, there is plenty of opportunity for reshuffling. Combined with a high rate of mutation at many of the individual sequences, this generates a mass of diversity from person to person and from place to place, as a reminder that to sequence a human genome is only a step in the much larger task of looking for differences among individuals. As some of the genes on chromosome six come in as many as two hundred forms the task will be a lengthy one; but it will be worthwhile because, for reasons unknown, some members of the defence force have the habit of turning on the body itself to give a range of auto-immune diseases such as rheumatoid arthritis, the skin disease psoriasis, and some forms of diabetes.

Whatever the details of its individual chromosomes, the picture to emerge from the completed human genome project is one of size, and ol complexity. Like the New World that stretched be!ore the first explorers, the genome is, above all, big; and like all large objects has a gravitational attraction for metaphors. Printed out, the information gathered by the Human Genome Project will fill two hundred telephone books or, in a single line, stretch the length of the Mississippi; a secretary would take twenty years to type (and a cantor fifty to sing) the whole thing, and so, symbolically, on.

Through all the symbolism and hyperbole is emerging an uneasy feeling that all this has been a race only to the starting line of understanding our genes and not to the winning post. The journal Nature reported the analysis of one of the very simplest viral genomes in the 1970s under the headline 'Sequencing is Not Enough'. That message emerges with renewed strength from the human genome project.

Even so, its completion is a milestone in the history of genetics. To look at an ancient chart — even one as faulty as that of Herodotus — is to realise that maps contain within themselves a great deal about the lives of those who drew them. They show the size and position of cities, the paths of migration, and the record of peoples long gone. The chart of the genes is made; and now the real journey can begin.