26 THE STUFF OF LIFE

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    IF YOUR TWO parents hadn’t bonded just when they did—possibly to the sed, possiblyto the nanosed—you wouldn’t be here. And if their parents hadn’t bonded in a preciselytimely manner, you wouldn’t be here either. And if their parents hadn’t done likewise, andtheir parents before them, and so on, obviously and indefinitely, you wouldn’t be here.

    Push backwards through time and these aral debts begin to add up. Go back just eightgeions to about the time that Charles Darwin and Abraham Lin were born, andalready there are over 250 people on whose timely couplings your existence depends.

    tinue further, to the time of Shakespeare and the Mayflower Pilgrims, and you have nofewer than 16,384 aors early exgiic material in a way that would,eventually and miraculously, result in you.

    At twenty geions ago, the number of people procreating on your behalf has risen to1,048,576. Five geions before that, and there are no fewer than 33,554,432 men andwomen on whose devoted couplings your existence depends. By thirty geions ago, yourtotal number of forebears—remember, these aren’t cousins and aunts and other ialrelatives, but only parents and parents of parents in a line leading iably to you—is overone billion (1,073,741,824, to be precise). If you go back sixty-feions, to the time ofthe Romans, the number of people on whose cooperative efforts your eventual existencedepends has risen to approximately 1,000,000,000,000,000,000, which is several thousandtimes the total number of people who have ever lived.

    Clearly something has gone wrong with our math here. The answer, it may i you tolearn, is that your line is not pure. You couldn’t be here without a little i—actually quitea lot of i—albeit at a geically discreet remove. With so many millions of aors inyour background, there will have been many occasions when a relative from your mother’sside of the family procreated with some distant cousin from your father’s side of the ledger. Infact, if you are in a partnership now with someone from your own rad try, theces are excellent that you are at some level related. Indeed, if you look around you on abus or in a park or café or any crowded place, most of the people you see are very probablyrelatives. When someone boasts to you that he is desded from William the queror orthe Mayflower Pilgrims, you should a once: “Me, too!” In the most literal andfual sense we are all family.

    We are also unily alike. pare yenes with any other human being’s and onaverage they will be about 99.9 pert the same. That is what makes us a species. The tinydifferences in that remaining 0.1 pert—“roughly one ide base ihousand,”

    to quote the British geicist a Nobel laureate John Sulston—are what endow uswith our individuality. Much has been made i years of the unraveling of the humangenome. In fact, there is no such thing as “the” human genome. Every human genome isdifferent. Otherwise we would all be identical. It is the endless rebinations of enomes—eaearly identical, but not quite—that make us what we are, both as individualsand as a species.

    But what exactly is this thing we call the genome? And what, e to that, are genes?

    Well, start with a cell again. Ihe cell is a nucleus, and inside eaucleus are theosomes—forty-six little bundles of plexity, of which twenty-three e from yourmother and twenty-three from your father. With a very few exceptions, every cell in yourbody—99.999 pert of them, say—carries the same plement of osomes. (Theexceptions are red blood cells, some immune system cells, and egg and sperm cells, which forvarious anizational reasons don’t carry the full geic package.) osomes stitutethe plete set of instrus necessary to make and maintain you and are made of longstrands of the little wonder chemical called deoxyribonucleic acid or DNA—“the mostextraordinary molecule oh,” as it has been called.

    Ds for just one reason—to create more DNA—and you have a lot of it inside you:

    about six feet of it squeezed into almost every cell. Each length of DNA prises some 3.2billioers of g, enough to provide 103,480,000,000possible binations, “guaraobe unique against all ceivable odds,” in the words of Christian de Duve. That’s a lot ofpossibility—a one followed by more than three billion zeroes. “It would take more than fivethousand average-size books just to print that figure,” notes de Duve. Look at yourself in themirror and reflect upon the fact that you are beholdihousand trillion cells, and thatalmost every one of them holds two yards of densely pacted DNA, and you begin toappreciate just how much of this stuff you carry around with you. If all your DNA werewoven into a single firand, there would be enough of it to stretch from the Earth to theMoon and baot once or twice but again and again. Altogether, acc to onecalculation, you may have as much as twenty million kilometers of DNA bundled up insideyou.

    Your body, in short, loves to make DNA and without it you couldn’t live. Yet DNA is notitself alive. No molecule is, but DNA is, as it were, especially unalive. It is “among the mostive, chemically i molecules in the living world,” in the words of the geicistRichard Lewontin. That is why it  be recovered from patches of long-dried blood or semenin murder iigations and coaxed from the bones of a Neaals. It also explainswhy it took stists so long to work out how a substanystifyingly low key—so, in aword, lifeless—could be at the very heart of life itself.

    As a knowy, DNA has been around lohan you might think. It was discoveredas far back as 1869 by Johann Friedrich Miescher, a Swiss stist w at the Uyof Tübingen in Germany. While delving microscopically through the pus in surgicalbandages, Miescher found a substance he didn’t reize and called it nu (because itresided in the nuclei of cells). At the time, Miescher did little more than s existence, butnu clearly remained on his mind, for twenty-three years later in a letter to his uncle heraised the possibility that such molecules could be the agents behind heredity. This was araordinary insight, but one so far in advance of the day’s stific requirements that itattracted no attention at all.

    For most of the  half tury the on assumption was that the material—nowcalled deoxyribonucleic acid, or DNA—had at most a subsidiary rol<cite>?</cite>e in matters of heredity. Itwas too simple. It had just four basipos, called ides, which was like havingan alphabet of just four letters. How could you possibly write the story of life with such arudimentary alphabet? (The answer is that you do it in much the way that you create plexmessages with the simple dots and dashes of Morse code—by bining them.) DNA didn’tdo anything at all, as far as anyone could tell. It just sat there in the nucleus, possibly bindingthe osome in some way or adding a splash of acidity on and or fulfilling someother trivial task that no one had yet thought of. The necessary plexity, it was thought,had to exist in proteins in the nucleus.

    There were, however, two problems with dismissing DNA. First, there was so much of it:

    two yards in nearly every nucleus, so clearly the cells esteemed it in some important way. Ontop of this, it kept turning up, like the suspe a murder mystery, in experiments. In twostudies in particular, one involving the Pneumonococcus bacterium and another involvingbacteriophages (viruses that i bacteria), Drayed an importahat could only beexplained if its role were more tral than prevailing thought allowed. The evidencesuggested that DNA was somehow involved in the making of proteins, a process vital to life,yet it was also clear that proteins were being made outside the nucleus, well away from theDNA that was supposedly direg their assembly.

    No one could uand how DNA could possibly be getting messages to the proteins. Theanswer, we now know, was RNA, or ribonucleic acid, which acts as an interpreter betweewo. It is a notable oddity of biology that DNA and proteins don’t speak the samelanguage. For almost four billion years they have been the living world’s great double act, ahey ao mutually inpatible codes, as if one spoke Spanish and the other Hindi.

    To unicate they need a mediator in the form of RNA. W with a kind of chemicalclerk called a ribosome, RNA translates information from a cell’s DNA into terms proteins uand and act upon.

    However, by the early 1900s, where we resume our story, we were still a very long wayfrom uanding that, or indeed almost anything else to do with the fused business ofheredity.

    Clearly there was a need for some inspired and clever experimentation, and happily the ageproduced a young person with the diligend aptitude to uake it. His name wasThomas Hunt Man, and in 1904, just four years after the timely rediscovery of Mendel’sexperiments with pea plants and still almost a decade befene would even bee a word,he began to do remarkably dedicated things with osomes.

    osomes had been discovered by  1888 and were so called because theyreadily absorbed dye and thus were easy to see uhe microscope. By the turn of thetweh tury it was strongly suspected that they were involved in the passing on of traits,but no one knew how, or even really whether, they did this.

    Man chose as his subject of study a tiny, delicate fly formally called Drosophilamelanogaster, but more only known as the fruit fly (or vinegar fly, banana fly, e fly). Drosophila is familiar to most of us as that frail, colorless ihat seems tohave a pulsive urge to drown in our drinks. As laboratory spes fruit flies had certainvery attractive advahey cost almost nothing to house and feed, could be bred by themillions in milk bottles, went from egg to productive parenthood in ten days or less, and hadjust four osomes, which kept things vely simple.

    W out of a small lab (which became knowably as the Fly Room) inSchermerhorn Hall at bia Uy in New York, Man and his team embarked ona program of meticulous breeding and crossbreeding involving millions of flies (onebiographer says billions, though that is probably an exaggeration), each of which had to becaptured with tweezers and examined under a jeweler’s glass for any tiny variations iance. For six years they tried to produce mutations by any means they could think of—zapping the flies with radiation and X-rays, rearing them in bright light and darkness, bakingthem gently in ovens, spinning them crazily irifuges—but nothing worked. Man wason the brink of giving up when there occurred a sudden aable mutation—a fly thathad white eyes rather than the usual red ones. With this breakthrough, Man and hisassistants were able to gee useful deformities, allowing them to track a trait throughsuccessive geions. By such means they could work out the correlatioweenparticular characteristid individual osomes, eventually proving to more or lesseveryone’s satisfa that osomes were at the heart of iance.

    The problem, however, remaihe  level of biological intricacy: the enigmatiesand the DNA that posed them. These were much trickier to isolate and uand. Aslate as 1933, when Man was awarded a Nobel Prize for his work, many researchers stillweren’t vihat genes eveed. As Man  the time, there was nosensus “as to what the genes are—whether they are real or purely fictitious.” It may seemsurprising that stists could struggle to accept the physical reality of something sofual to cellular activity, but as Wallace, King, and Sanders point out in Biology: TheSce of Life (that rarest thing: a readable college text), we are in much the same positiontoday with mental processes such as thought and memory. We know that we have them, ofcourse, but we don’t know what, if any, physical form they take. So it was for the loimewith gehe idea that you could plue from your body and take it away for study wasas absurd to many of Man’s peers as the idea that stists today might capture a straythought and exami under a microscope.

    What was certainly true was that something associated with osomes was diregcell replication. Finally, in 1944, after fifteen years of effort, a team at the RockefellerInstitute in Manhattan, led by a brilliant but diffident adian named Oswald Avery,succeeded with an exceedingly tricky experiment in whi innocuous strain of bacteria ermaly iious by crossing it with alien DNA, proving that DNA was far morethan a passive molecule and almost certainly was the active agent in heredity. The Austrian-born biochemist Erwin Chargaff later suggested quite seriously that Avery’s discovery wasworth two Nobel Prizes.

    Unfortunately, Avery posed by one of his own colleagues at the institute, a strong-willed and disagreeable proteihusiast named Alfred Mirsky, who did everything in hispower to discredit Avery’s work—including, it has been said, lobbying the authorities at theKarolinska Institute in Sto not to give Avery a Nobel Prize. Avery by this time wassixty-six years old and tired. Uo deal with the stress and troversy, he resigned hisposition and never went near a lab again. But other experiments elsewhere overwhelminglysupported his clusions, and soon the race was on to find t<dfn>..</dfructure of DNA.

    Had you been a betting person in the early 1950s, your money would almost certainly havebeen on Linus Pauling of Caltech, America’s leading chemist, to crack the structure of DNA.

    Pauling was unrivaled iermining the architecture of molecules and had been a pioneer inthe field of X-ray crystallography, a teique that would prove crucial to peering into theheart of DNA. In an exceedingly distinguished career, he would win two Nobel Prizes (forchemistry in 1954 and pea 1962), but with DNA he became vihat the structurewas a triple helix, not a double one, and never quite got on the right track. Instead, victory fellto an unlikely quartet of stists in England who didn’t work as a team, often weren’t onspeaking terms, and were for the most part novices in the field.

    Of the four, the o a ventional boffin was Maurice Wilkins, who had spent muchof the Sed World War helping to desigomib. Two of the others, RosalindFranklin and Francis Crick, had passed their war years w on mines for the Britishgover—Crick of the type that blow up, Franklin of the type that produce coal.

    The most unventional of the foursome was James Watson, an Ameri prodigy whohad distinguished himself as a boy as a member of a highly popular radiram called TheQuiz Kids (and thus could claim to be at least part of the inspiration for some of the membersof the Glass family in Franny and Zooey and other works by J. D. Salinger) and who hadehe Uy of Chicago aged just fifteen. He had earned his Ph.D. by the age oftwenty-two and was now attached to the famous dish Laboratory in Cambridge. In1951, he was a gawky twenty-three-year-old with a strikingly lively head of hair that appearsin photographs to be straining to attach itself to some powerful mag just out of frame.

    Crick, twelve years older and still without a doctorate, was less memorably hirsute andslightly more tweedy. In Watson’s at he is presented as blustery, nosy, cheerfullyargumentative, impatient with anyone slow to share a notion, and stantly in danger ofbeing asked to go elsewhere. her was formally trained in biochemistry.

    Their assumption was that if you could determihe shape of a DNA molecule you wouldbe able to see—correctly, as it turned out—how it did what it did. They hoped to achieve this,it would appear, by doing as little work as possible beyond thinking, and no more of that thanwas absolutely necessary. As Watson cheerfully (if a touch disingenuously) remarked in hisautobiographical book The Double Helix, “It was my hope that the gene might be solvedwithout my learning any chemistry.” They weren’t actually assigo work on DNA, and atone point were ordered to stop it. Watson was ostensibly mastering the art of crystallography;Crick was supposed to be pleting a thesis on the X-ray diffra of large molecules.

    Although Crid Watson enjoy nearly all the credit in popular ats for solving themystery of DNA, their breakthrough was crucially depe on experimental work doheir petitors, the results of which were obtained “fortuitously,” iactful words of thehistorian Lisa Jardine. Far ahead of them, at least at the beginning, were two academics atKing’s College in London, Wilkins and Franklin.

    The New Zealand–born Wilkins was a retiring figure, almost to the point of invisibility. A1998 PBS dotary on the discovery of the structure of DNA—a feat for which he sharedthe 1962 Nobel Prize with Crid Watson—mao overlook him entirely.

    The most enigmatic character of all was Franklin. In a severely unflattering portrait,Watson in The Double Helix depicted Franklin as a woman who was unreasonable, secretive,ically uncooperative, and—this seemed especially to irritate him—almost willfullyunsexy. He allowed that she “was not unattractive and might have been quite stunning had shetaken even a mild i in clothes,” but in this she disappointed all expectations. She didn’teven use lipstick, he noted in wonder, while her dress sense “showed all the imagination ofEnglish blue-stog adolests.”

    1However, she did have the best images ience of the possible structure of DNA,achieved by means of X-ray crystallography, the teique perfected by Linus Pauling.

    Crystallography had been used successfully to map atoms in crystals (hence“crystallography”), but DNA molecules were a much more finicky proposition. Only Franklinwas managing to get good results from the process, but to Wilkins’s perennial exasperationshe refused to share her findings.

    If Franklin was not warmly forthing with her findings, she ot be altogetherblamed. Female academics at King’s in the 1950s were treated with a formalized disdain thatdazzles modern sensibilities (actually any sensibilities). However senior or aplished,they were not allowed into the college’s senior on room but instead had to take theirmeals in a more utilitarian chamber that even Watson ceded was “dingily pokey.” On topof this she was being stantly pressed—at times actively harassed—to share her results witha trio of men whose desperation to get a peek at them was seldom matched by more engagingqualities, like respect. “I’m afraid we always used to adopt—let’s say a patronizing attitudetoward her,” Crick later recalled. Two of these men were from a peting institution and thethird was more or less openly siding with them. It should hardly e as a surprise that shekept her results locked away.

    That Wilkins and Franklin did not get along was a fact that Watson and Crick seem to haveexploited to their be. Although Crid Watsorespassing rather unashamedlyon Wilkins’s territory, it was with them that he increasingly sided—not altogether surprisinglysince Franklin herself was beginning to a a decidedly queer way. Although her resultsshowed that DNA definitely was helical in shape, she insisted to all that it was not. ToWilkins’s presumed dismay and embarrassment, in the summer of 1952 she posted a mootice around the King’s physics department that said: “It is with great regret that we have toannouhe death, on Friday 18th July 1952 of D.N.A. helix. . . . It is hoped that Dr. M.H.F.

    Wilkins will speak in memory of the late helix.”

    The oute of all this was that in January 1953, Wilkins showed Watson Franklin’simages, “apparently without her knowledge or sent.” It would be an uatement to callit a signifit help. Years later Watson ceded that it “was the key event . . . it mobilizedus.” Armed with the knowledge of the DNA molecule’s basic shape and some importas of its dimensions, Watson and Crick redoubled their efforts. Everything now seemedto go their way. At one point Pauling was en route to a feren England at which hewould in all likelihood have met with Wilkins and learned enough to correct themisceptions that had put him on the wrong line of inquiry, but this was the McCarthy eraand Pauling found himself detai Idlewild Airport in New York, his passport fiscated,on the grounds that he was too liberal of temperament to be allowed to travel abroad. Crid Watson also had the no less ve good fortuhat Pauling’s son was w atthe dish and ily kept them abreast of any news of developments abacks athome.

    Still fag the possibility of being trumped at any moment, Watson and Crick appliedthemselves feverishly to the problem. It was known that DNA had four chemical1In 1968, Harvard Uy Press celed publication of The Double Helix after Crid Wilkinsplained about its characterizations, which the sce historian Lisa Jardine has described as &quot;gratuitouslyhurtful.&quot; The descriptions quoted above are after Watson softened his ents.

    pos—called adenine, guanine, cytosine, and thiamine—and that these paired up inparticular ways. By playing with pieces of cardboard cut into the shapes of molecules, Watsonand Crick were able to work out how the pieces fit together. From this they made a Meo-like model—perhaps the most famous in modern sce—sisting of metal plates boltedtogether in a spiral, and invited Wilkins, Franklin, and the rest of the world to have a look.

    Any informed person could see at ohat they had solved the problem. It was withoutquestion 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.” Apanying it were separate articles byWilkins and Franklin. It was aful time in the world—Edmund Hillary was just about toclamber to the top of Everest while Elizabeth II was immily to be ed queen ofEngland—so the discovery of the secret of life was mostly overlooked. It received a smallmention in the News icle and was ignored elsewhere.

    Rosalind Franklin did not share in the Nobel Prize. She died of ovarian cer at the age ofjust thirty-seven in 1958, four years before the award was granted. Nobel Prizes are notawarded posthumously. The cer almost certainly arose as a result of ic overexposureto X-rays through her work and  have happened. In her much-praised 2002 biographyof Franklin, Brenda Maddox hat Franklin rarely wore a lead apron and often steppedcarelessly in front of a beam. Oswald Avery never won a Nobel Prize either and was alsely overlooked by posterity, though he did at least have the satisfa of living just longenough to see his findings vindicated. He died in 1955.

    Watson and Crick’s discovery wasn’t actually firmed until the 1980s. As Crick said inone of his books: “It took over twenty-five years for our model of DNA to go from being onlyrather plausible, to being very plausible . . . and from there to being virtually certainlycorrect.”

    Even so, with the structure of DNA uoress iics was swift, and by 1968the journal Sce 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 geics was nearly at anend.

    In fact, of course, it was only just beginning. Even now there is a great deal about DNA thatwe scarcely uand, not least why so much of it doesn’t actually seem to do anything.

    y-seven pert of your DNA sists of nothing but long stretches of meaninglessgarble—“junk,” or “non-g DNA,” as biochemists prefer to put it. Only here and therealong each strand do you fiions that trol and aal funs. These are thecurious and long-elusive genes.

    Genes are nothing more (nor less) than instrus to make proteins. This they do with acertain dull fidelity. In this sehey are rather like the keys of a piano, each playing asie and nothing else, which is obviously a trifle monotonous. But bihe genes,as you would bine piano keys, and you  create chords and melodies of infinite variety.

    Put all these geogether, and you have (to tihe metaphor) the great symphony ofexistenown as the human genome.

    An alternative and more on way tard the genome is as a kind of instruanual for the body. Viewed this way, the osomes  be imagined as the book’schapters and the genes as individual instrus for making proteins. The words in which theinstrus are written are called s, and the letters are know<s>９9ｌｉｂ?</s>n as bases. The bases—theletters of the geic alphabet—sist of the four ides mentioned a page or two back:

    adehiamine, guanine, and cytosine. Despite the importance of what they do, thesesubstances are not made of anythiic. Guanine, for instance, is the same stuff thatabounds in, and gives its o, guano.

    The shape of a DNA molecule, as everyone knows, is rather like a spiral staircase ortwisted rope ladder: the famous double helix. The uprights of this structure are made of a typeof sugar called deoxyribose, and the whole of the helix is a nucleic acid—hehe name“deoxyribonucleic acid.” The rungs (or steps) are formed by two bases joining across thespace between, and they  bine in only two ways: guanine is alaired withcytosine and thiamine always with adehe order in which these letters appear as youmove up or down the ladder stitutes the DNA code; logging it has been the job of theHuman Genome Project.

    Now the particular brilliance of DNA lies in its manner of replication. When it is time toproduce a new DNA molecule, the two strands part down the middle, like the zipper on ajacket, and each half goes off to form a new partnership. Because eaucleotide along astrand pairs up with a specific other ide, each strand serves as a template for thecreation of a new matg strand. If you possessed just orand of your own DNA, youcould easily enough restruct the matg side by w out the necessary partnerships:

    if the topm orand was made of guahen you would know that thetopm og strand must be cytosine. Work your way down the ladderthrough all the ide pairings, aually you would have the code for a newmolecule. That is just what happens in nature, except that nature does it really quickly—inonly a matter of seds, which is quite a feat.

    Most of the time our DNA replicates with dutiful accuracy, but just occasionally—aboutoime in a million—a letter gets into the wrong place. This is known as a single idepolymorphism, or SNP, familiarly known to biochemists as a “Snip.” Generally these Snipsare buried in stretches of nong DNA and have able sequence for the body.

    But occasionally they make a differehey might leave you predisposed to some disease,but equally they might fer some slight advantage—more protective pigmentation, forinstance, or increased produ of red blood cells for someone living at altitude. Over time,these slight modifications accumulate in both individuals and in populations, tributing tothe distinctiveness of both.

    The balaween accurad errors in replication is a fine ooo many errors andthe anism ’t fun, but too few and it sacrifices adaptability. A similar balance mustexist between stability in an anism and innovation. An increase in red blood cells  helpa persroup living at high elevations to move and breathe more easily because more redcells  carry more oxygen. But additional red cells also thi the blood. Add too many,and “it’s like pumping oil,” in the words of Temple Uy anthropologist Charles Weitz.

    That’s hard on the heart. Thus those desigo live at high altitude get increased breathingefficy, but pay for it with higher-risk hearts. By such means does Darwinian naturalsele look after us. It also helps to explain why we are all so similar. Evolution simplywon’t let you bee too different—not without being a new species anyway.

    The 0.1 pert differeween yenes and mine is ated for by our Snips.

    Now if you pared your DNA with a third person’s, there would also be 99.9 pertcorrespondence, but the Snips would, for the most part, be in different places. Add morepeople to the parison and you will get yet more Snips i more places. For every one ofyour 3.2 billion bases, somewhere on the plahere will be a person, roup of persons,with different g in that position. So not only is it wrong to refer to “the” human ge in a sense we don’t even have “a” human genome. We have six billion of them. We are all99.9 pert the same, but equally, in the words of the biochemist David Cox, “you could sayall humans share nothing, and that would be correct, too.”

    But we have still to explain why so little of that DNA has any disible purpose. It startsto get a little unnerving, but it does really seem that the purpose of life is to perpetuate DNA.

    The 97 pert of our DNA only called junk is largely made up of clumps of lettersthat, in Ridley’s words, “exist for the pure and simple reason that they are good at gettingthemselves duplicated.”

    2Most of your DNA, in other words, is not devoted to you but toitself: you are a mae for reprodug it, not it for you. Life, you will recall, just wants tobe, and DNA is what makes it so.

    Even when DNA includes instrus for making genes—when it codes for them, asstists put it—it is not necessarily with the smooth funing of the anism in mind.

    One of the o genes we have is for a protein called reverse transcriptase, which hasno known beneficial fun in human beings at all. The ohing itdoes do is make itpossible for retroviruses, such as the AIDS virus, to slip unnoticed into the human system.

    In other words, our bodies devote siderable energies to produg a protein that doesnothing that is beneficial and sometimes clobbers us. Our bodies have no choice but to do sobecause the genes order it. We are vessels for their whims. Altogether, almost half of humahe largest proportio found in any anism—don’t do anything at all, as far aswe  tell, except reproduce themselves.

    All anisms are in some sense slaves to their gehat’s why salmon and spiders andother types of creatures more or less beyond ting are prepared to die in the process ofmating. The desire to breed, to disperse one’s genes, is the most powerful impulse in nature.

    As Sherwin B. Nuland has put it: “Empires fall, ids explode, great symphonies are written,and behind all of it is a single instinct that demands satisfa.” From an evolutionary pointof view, sex is really just a reward meism to ence us to pass on eic material.

    Stists had only barely absorbed the surprisihat most of our DNA doesn’t doanything when even more ued findings began to turn up. First in Germany and then inSwitzerland researchers performed some rather bizarre experiments that produced curiouslyunbizarre outes. Ihey took the gehat trolled the development of a mouse’seye and ied it into the larva of a fruit fly. The thought was that it might produething iingly grotesque. In fact, the mouse-eye ge only made a viable eye inthe fruit fly, it made a fly’s eye. Here were two creatures that hadn’t shared a oor for 500 million years, yet could s geic material as if they were sisters.

    The story was the same wherever researchers looked. They found that they could ihuman DNA into certain cells of flies, and the flies would accept it as if it were their own.

    2Junk DNA does have a use. It is the portion employed in DNA fingerprinting. Its practicality for this purposewas discovered actally by Alec Jeffreys, a stist at the Uy of Leicester in England. In 1986Jeffreys was studying DNA sequences feic markers associated with heritable diseases when he roached by the polid asked if he could help ect a suspect to two murders. He realized his teiqueought to work perfectly for solving criminal cases-and so it proved. A young baker with the improbable name of Pitchfork was senteo two life terms in prison for the murders.

    Over 60 pert of human genes, it turns out, are fually the same as those found infruit flies. At least 90 pert correlate at some level to those found in mice. (We even havethe same genes for making a tail, if only they would swit.) In field after field,researchers found that whatever anism they were w oher ode wormsor human beings—they were often studying essentially the same genes. Life, it appeared, wasdrawn up from a si of blueprints.

    Further probings revealed the existence of a clutaster trol genes, each diregthe development of a se of the body, which were dubbed homeotic (from a Greek wordmeaning “similar”) or hox genes. Hox genes answered the long-bewildering question of howbillions of embryonic cells, all arising from a single fertilized egg and carrying identiA, know where to go and what to do—that this one should bee a liver cell, this oreteuron, this one a bubble of blood, this one part of the shimmer on a beating wing. Itis the hox gehat instruct them, and they do it for all anisms in much the same way.

    Iingly, the amount of geic material and how it is anized doesn’t necessarily, oreven generally, reflect the level of sophistication of the creature that tains it. We haveforty-six osomes, but some ferns have more than six huhe lungfish, one of theleast evolved of all plex animals, has forty times as muA as we have. Even theo is meically splendorous than we are, by a factor of five.

    Clearly it is not the number of genes you have, but what you do with them. This is a verygood thing because the number of genes in humans has taken a big hit lately. Until retly itwas thought that humans had at least 100,000 genes, possibly a good many more, but thatnumber was drastically reduced by the first results of the Human Genome Project, whichsuggested a figure more like 35,000 or 40,000 genes—about the same number as are found ingrass. That came as both a surprise and a disappoi.

    It won’t have escaped your attention that genes have been only implicated in anynumber of human frailties. Exultant stists have at various times declared themselves tohave found the genes responsible for obesity, schizophrenia, homosexuality, criminality,violence, al, even shoplifting and homelessness. Perhaps the apogee (or nadir) of thisfaith in biodeterminism was a study published in the journal S 1980 tending thatwomen are geically inferior at mathematics. In fact, we now know, almost nothing aboutyou is so aodatingly simple.

    This is clearly a pity in one important sense, for if you had individual gehat determi or propensity to diabetes or to baldness or any other distinguishing trait, then it wouldbe easy—paratively easy anyway—to isolate and tinker with them. Unfortunately, thirty-five thousand genes funing indepely is not nearly enough to produce the kind ofphysical plexity that makes a satisfactory human being. Genes clearly therefore mustcooperate. A few disorders—hemophilia, Parkinson’s disease, Huntington’s disease, andcystic fibrosis, for example—are caused by lone dysfunal genes, but as a rule disruptivegenes are weeded out by natural sele long before they  bee permalytroublesome to a species or population. For the most part our fate and fort—and even oureye color—are determined not by individual genes but by plexes of genes w inalliahat’s why it is so hard to work out how it all fits together and on’t beprodug designer babies anytime soon.

    In fact, the more we have learned i years the more plicated matters have teo bee. Even thinking, it turns out, affects the ways genes work. How fast a man’s beardgrows, for instance, is partly a fun of how much he thinks about sex (because thinkingabout sex produces a testosterone surge). In the early 1990s, stists made an even moreprofound discovery when they found they could knock out supposedly vital genes fromembryonic mice, and the mice were not only often borhy, but sometimes were actuallyfitter than their brothers and sisters who had not been tampered with. Wheain importantgenes were destroyed, it turned out, others were stepping in to fill the breach. This wasexcellent news for us as anisms, but not so good for our uanding of how cells worksi introduced ara layer of plexity to something that we had barely begun touand anyway.

    It is largely because of these plig factors that crag the human genome becameseen almost at once as only a beginning. The genome, as Erider of MIT has put it, is likea parts list for the human body: it tells us what we are made of, but says nothing about hoork. What’s needed now is the operating manual—instrus for how to make it go.

    We are not close to that poi.

    So now the quest is to crack the human proteome—a cept so hat the termproteome didn’t eve a decade ago. The proteome is the library of information thatcreates proteins. “Unfortunately,” observed Stific Ameri in the spring of 2002, “theproteome is much more plicated than the genome.”

    That’s putting it mildly. Proteins, you will remember, are the workhorses of all livingsystems; as many as a hundred million of them may be busy in any cell at any moment. That’sa lot of activity to try to figure out. Worse, proteins’ behavior and funs are based notsimply on their chemistry, as with genes, but also on their shapes. To fun, a protein mustnot only have the necessary chemical pos, properly assembled, but then must also befolded into aremely specific shape. “Folding” is the term that’s used, but it’s amisleading one as it suggests a geometrical tidihat doesn’t in fact apply. Proteins loopand coil and kle into shapes that are at oravagant and plex. They are more likefuriously mangled coat hahan folded towels.

    Moreover, proteins are (if I may be permitted to use a handy archaism) the swingers of thebiological world. Depending on mood aabolic circumstahey will allowthemselves to be phosphorylated, glycosylated, acetylated, ubiquitinated, farneysylated,sulfated, and lio glycophosphatidylinositol anchors, among rather a lot else. Often ittakes relatively little to get them going, it appears. Drink a glass of wine, as StificAmeriotes, and you materially alter the number and types of proteins at large in yoursystem. This is a pleasaure for drinkers, but not nearly so helpful feicists who aretrying to uand what is going on.

    It  all begin to seem impossibly plicated, and in some ways itis impossiblyplicated. But there is an underlying simplicity in all this, too, owing to an equallyelemental underlying unity in the way life works. All the tiny, deft chemical processes thatanimate cells—the cooperative efforts of ides, the transcription of DNA into RNA—evolved just ond have stayed pretty well fixed ever since across the whole of nature. Asthe late French geicist Jacques Monod put it, only half i: “Anything that is true of E.

    ust be true of elephants, except more so.”

    Every living thing is an elaboration on a single inal plan. As humans we are mereis—each of us a musty archive of adjustments, adaptations, modifications, andprovidential tinkerings stretg back 3.8 billion years. Remarkably, we are even quiteclosely related to fruit aables. About half the chemical funs that take pla abanana are fually the same as the chemical funs that take pla you.

    It ot be said too often: all life is ohat is, and I suspect will forever prove to be, themost profound true statement there is.

    PART  VITHE ROAD TO USDesded from the apes! My dear,let us hope that it is not true, but if it is,let us pray that it will not beegenerally known.

    -Remark attributed to the wife ofthe Bishop of Worcester afterDarwin’s theory of evolution was Explaio her

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