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The Private View

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Welcome to the chromosome portrait gallery.

Scientific papers traditionally end with a “Discussion” section, and the temptation here is to follow that convention and write a final chapter that summarizes the rest of the book and comes up with ponderous conclusions. But that is not how road movies end, is it? Most of the time the protagonists never get to their destination and end up, like Peter Fonda and Dennis Hopper in Easy Rider, blasted by a shotgun and dead at the side of the road. Even if I was feeling the worse for wear at the end of three months on the move, my chest was only wheezy, not full of lead shot.

I did return with Ulla to the United States six months later, carrying with me an armful of chromosome portraits and ready to go through them with my volunteers. Time and money confined the face-to-face meetings to the east coast, so I sent individual chromosome portraits to everyone else by snail- or e-mail, and followed up with a phone call. I had asked the volunteers to make a stab at what they thought their own portrait might look like before I showed it to them, and then observed how they reacted when the canvas was revealed. The journalist in me was waiting for a series of dramatic outbursts when expectations met reality, but there were none. Most of the time my volunteers either declined to hazard a guess or, when they did, found that it more or less matched what their portraits revealed. When it did not, the reactions were muted and reflective rather than indignant. But what do the portraits look like? I will let them speak for themselves.

Welcome to the “Private View.” Take a glass of champagne in one hand and a canapé in the other. Think of this last chapter as the catalog. Go to the color insert section and take your time to browse.

The first portrait in the gallery is of my New England volunteer “Margo Channing.” She is, as you see, all one color: blue. This means that without a single exception, all of “Margo”’s DNA has a European origin. It is not the most colorful portrait or, you might think, the best to choose to begin our tour of the gallery. More Rothko than Magritte. But, despite its uniformity, this portrait is one of the most interesting and surprising of all. I could equally well have shown you the portraits of my other New England volunteers: “Terry Malloy,” “Rio McDonald,” “Anna Christie,” “Lisa Fremont,” or “Rose Sayer.”* All of them are exactly the same, solidly blue throughout without a trace of DNA from either African or Native American ancestors. Remember that all my sitters in this part of the gallery are descended from European settlers who arrived in New England during the seventeenth century, many of them before 1650. And yet there is not the slightest echo of any interbreeding with Native Americans, with whom they lived in close proximity. Had there been, then the blue chromosomes would have been flecked with orange. That was what I had been expecting, having seen the effects of European settlement among other indigenous people where genes are quick to cross ethnic boundaries in both directions. But in New England there is no sign of it.

I can only conclude that, if there had been any intermixing between early New Englanders and the indigenous tribes living around Plymouth and Cape Cod, the offspring would have stayed within the Indian tribes rather than being absorbed into the English settlements. The single exception is “Atticus Finch.” His portrait shows a tiny fleck of orange at the end of chromosome 9.

“Atticus,” if you recall, had reason to believe he was descended on his father’s side from Ots-Toch, the daughter of a Mohawk mother and a French father. Although I cannot prove it beyond any doubt, I think it likely that the speck of orange in “Atticus”’s chromosome portrait really is the genetic legacy that he inherited directly from Ots-Toch and her Mohawk mother. The fact that the portraits of my other New England volunteers were all uniformly European blue throughout makes me think that the little bit of orange in “Atticus Finch”’s portrait is genuinely from his Mohawk ancestor. After twelve generations of doubling dilution, there was never going to be much left of her DNA in “Atticus”’s genome, and the single speck we see in his portrait is about all I would have expected.

One of the attractions that drew me to the chromosome portraits, as well as their visual impact, is that it is easy to look up which genes correspond to which particular chromosome segments. The Human Genome Project located all our genes at fixed points along the chromosomes, so it is a simple task in “Atticus Finch”’s case to identify which genes have come down to him from Ots-Toch. This will identify the parts of “Atticus”’s body that are running on Mohawk DNA. Among several genes that chromosome 9 carries with frankly obscure functions, there is one that is familiar to all of us. This is the gene that controls our blood group, deciding whether we are group A, B, AB or O. We all have two copies of this gene, one from each parent, and in “Atticus”’s case one of them has been inherited from Ots-Toch, while the other has come from a European ancestor on his mother’s side of the family. Both Mohawk and European genes are working together to decide “Atticus”’s blood group, and since he is fit and well, it looks as though they are doing a good job.

“Harry Lime,” a staff member at the New England Historic Genealogy Society who also volunteered to have his chromosomes painted, was the only other European New Englander to have anything other than a uniformly blue chromosome portrait. In his case, as you can see, the speck of color was not orange but green. “Harry Lime” therefore has an African ancestor. When I unveiled the portrait, his first question—to himself more than to me—was to wonder who this ancestor might have been. Being a professional genealogist, he set off in search of this unexpected family member. Like “Atticus Finch”’s portrait, this was only a splash of color amid a sea of blue, suggesting that, whoever it was, his African ancestor had lived a very long time ago. The likelihood is that he or she was an African American, but even that is not certain. Some Europeans, myself included, have small segments of African DNA that must have entered the British gene pool at some time in the past. The last time I spoke to “Harry,” he was still on the track of his elusive African ancestor.

As we did with “Atticus Finch,” we can also see which of “Harry”’s genes are firing on African DNA. The section of chromosome 7 containing African DNA does not hold any well-known genes. However, there is one intriguing gene among the otherwise uninspiring collection. It belongs to the family of genes that control the exquisitely sensitive receptors that give us our sense of smell. It is a large family dispersed around the human genome, with each member of the family capable of sensing particular odors. In “Harry”’s case one of these is being run by a collaboration of DNA from one African and one European ancestor.

For proof that Britons can also have African DNA, we need look no further than my own chromosome portrait. As you can see, it has a small segment of green at the tip of chromosome 11. I don’t know which ancestor this has come from, but black Africans have been coming to Britain since at least the time of the Roman Empire. Indeed there was an influx of African Americans who moved to Britain after the Revolutionary War, having been persuaded to fight on the British side with a promise of a guaranteed welcome in England after the war was over. In fact the promise was never kept, and most were shipped off to Nova Scotia, although some did eventually make their way to Britain. So, while my African ancestor probably came to Britain a very long time ago as a Roman slave, he or she might instead have been an African American, just as “Harry”’s African ancestor could have been British.

The particular segment of African chromosome 11 that I have inherited happens to be very rich in genes. Among many others, there are genes for insulin and for beta-globin, one of the two subunits of hemoglobin located there. So both my body’s pancreatic insulin and hemoglobin output are controlled by a fifty-fifty mixture of African and European DNA. I also have a fleck of orange from an unknown Asian ancestor, and the segment of chromosome 7 that contains it houses an important collagen gene. So my skin and bones owe a great deal of their mechanical strength to my Asian ancestor, just as much as my pancreas is jointly run on African DNA.

Judging by her portrait, “Phyllis Dietrichson,” like “Harry Lime,” also has an African ancestor and although I met her through the NEHGS headquarters in Boston, some of her family are from North Carolina. Like “Harry,” she does not know who this African ancestor was, but she was delighted when I told her that the chromosomal segment involved, which as you can see is located on her chromosome number 7, contains an important muscle gene called beta-actin. With this new knowledge, “Phyllis” now flexes her African biceps with increased vigor.

On our travels around America we met with “Rhett Butler,” and, thanks to Ulla’s powers of persuasion, before long we had a sample of his DNA. “Rhett” was a European American from the South, from Georgia, whose ancestors had come over from England in the early eighteenth century. He was quite sure he did not have any black ancestors, but when his portrait came back, there were three streaks of green against an otherwise all-blue genome. His reaction to this when I showed him was amusement more than anything else. By the sound of it, his sister had married a man who was a bit of a racist, and “Rhett” was looking forward to telling him that he had actually married a black woman, on the very reasonable assumption that at least some of his African ancestor’s genes had also been inherited by his sister.

The portrait of another of our volunteers, “Sugar Kane,” also shows up several long segments of African DNA. If you recall, Ulla and I met “Sugar” and her husband in San Francisco, where she had told us about the family photograph of her grandmother who looked to her like a Native American. It was because of the possibility of an Indian ancestor that “Sugar” had become very interested in the spiritual life of Native Americans and had gone on her own spirit quest, including a spell in the sweat lodge at Pine Ridge. “Sugar” and her family had lived in Florida for generations, and from the appearance of her chromosome portrait, she certainly does have one or more black ancestors. If you look closely you will see that she also has two very short smudges of orange from what was very probably a Native American ancestor. There isn’t enough there to indicate that the grandmother in her family album was a full-blooded American Indian, but as we shall see, that is not always easy to tell from a genetic analysis.

Our other volunteer who, like “Sugar Kane,” certainly considered herself to be from solidly European stock was “Ilsa Lund.” Appropriately enough “Ilsa”’s family hails from the Carolinas, and her chromosome portrait—the one that gave Joanna Mountain such a shock when she first saw it—has even more green segments than “Sugar Kane”’s. As you see, the green segments in “Ilsa”’s portrait are quite long and relatively intact, which suggests they have been inherited from a fairly recent African ancestor. That is because there has been less time for the segments to be broken up by the constant shuffling that chromosomes undergo between each generation. However, despite having her cousin Greg on the case, the last time we spoke, “Ilsa” had been unable to identify any black ancestors in the family. Tellingly, she has not let her mother know. Like “Sugar Kane,” “Ilsa”’s portrait also has the tiniest flecks of orange on four of her chromosomes, indicating a far distant Native American ancestry as well.

I am the first to point out that the gallery has far too small a number of individual portraits for me to draw any statistically significant conclusions. But that isn’t going to stop me making a few observations on the collection for the catalog notes. I am genuinely astonished to find so little genetic evidence of intermixing among the descendants of the early New England settlers. Of the twelve complete genome scans, each one scrutinizing half a million markers, I found a segment of orange only in “Atticus Finch”’s portrait, and he probably inherited it from the Mohawk ancestor he knew about. Apart from the one segment of African DNA in “Harry Lime,” every other New Englander has a completely European set of chromosomes. The volunteers themselves were not as surprised as I was, but I think that is only to be expected. After all, none of the European American volunteers from the South thought they had any African ancestors, yet they all did. The only explanation I can come up with for the completely blue portraits from New England is that if there were any liaisons with Native Americans, the offspring were never, or almost never, accepted into the English colonies and instead were raised as Indians.

Again with far too little to go on, the observation that all my white volunteers from the South did have at least some African genetic ancestry is in such stark contrast to New England that I think it is probably a genuine finding. Of course, the irony of the “one-drop” rule, which condemned anyone with the least bit of black ancestry to the life of a slave, is highlighted by the implication from these DNA results that many whites with deep roots in the South have some black ancestors.

The portraits of my European American volunteers had produced fascinating results, even if the portraits themselves were rather monotone, being mostly blue with the very occasional brushstroke of green and orange. This all changed when I unwrapped the portraits from my African American DNA sitters, which you will see as, catalog in hand, we make our way to the next room in the chromosome gallery.

In this section of the exhibition you can see portraits with a full range of color from the almost all-green Toby Cooper, through blue on green in “Virgil Tibbs”’s chromosomes, to the balanced blend of blue and green in the portrait of Mark Thompson. However, as you can see at a glance, unlike the New Englanders, not one of the portraits of my African American volunteers has a completely uniform set of chromosomes. Every single one shows the genetic evidence of at least some European ancestry. The other feature to notice in this section of the gallery is that all of the African American portraits also show some blocks of orange from Native American ancestors. There are some aspects of the brushwork that I think may indicate slight inaccuracies in assigning the Native American component against an otherwise African background. To be more precise, I am surprised that so many of the orange segments among African Americans extend across both chromosomes, which if taken literally would mean that they had been inherited from a common ancestor, which I find most unlikely. But this is only a detail and does not diminish the observation that all the chromosome portraits of my African American volunteers have some degree of Native American ancestry. This news delighted many of my volunteers who, like “Virgil Tibbs” from Boston, had hoped for a tangible genetic link to the indigenous inhabitants of their adopted land. Another notable feature of the collection is that the chromosome portraits of my African American sitters from the South, like Toby Cooper and the two friends from Atlanta, “Ned Land” and “Mildred Pierce,” have a lot more green in them than the portraits of their fellow African Americans, like Mark Thompson and “Virgil Tibbs,” whose ancestors had moved north either directly after the Civil War or later on in the nineteenth century.

Moving to the final section of the gallery, I have already explained why I did not want to paint the genetic portraits of Native Americans for DNA USA. However, I was fortunate to meet up with “Will Kane” and “Roger Thornhill,” who each had one Native American and one European parent and who were gracious enough to give DNA samples. When I unwrapped the paintings prior to displaying them, I could see, as you can, that both portraits have a large component of blue from their European parents. However, the way the portraits are painted means that this contribution can easily be subtracted, leaving the lower half of each chromosome representing the Native American component. In both “Will”’s and “Roger”’s portraits you can see that these lower segments are a mixture of blue and orange. We have seen earlier in the book that although portraits of Native American chromosomes appear to have a European component, this can be partly due to the Asia/Europe border artifacts of Siberian chromosomes rather than a genuinely recent European admixture. Mike MacPherson’s estimate is that chromosome portraits of Native Americans living five hundred years ago, before there was any chance of interbreeding with recently arrived Europeans, would be 75 +/– 15 percent orange with the remainder blue. On these grounds the Navajo and Hopi ingredients of “Will Kane”’s and “Roger Thornhill”’s genome are well within the range for unmixed Native American chromosomes. What is noticeable is that there are no signs of green, meaning African ancestry, in either of the portraits.

“Will”’s Navajo and “Roger”’s Hopi chromosomes contrast dramatically with the final portrait in this room from my one and only Cherokee volunteer, “Lucas Jackson.” I was astonished when I first saw his chromosome portrait, and so was he. “Isn’t that something!” he said with quiet amazement. There is only one small segment of orange among an otherwise uniform sea of blue. I would have dismissed this as an error were it not for something Mike MacPherson said when I visited him in San Francisco. He had evidently had a similar experience with the company’s Cherokee customers, and had often found very little sign of orange in their chromosome portraits. We did not discuss the “Cherokee paradox,” as MacPherson called it, any more than that, but it did make me think that perhaps “Lucas Jackson”’s portrait was not so unusual for a Cherokee as I had first thought. It also shone an admittedly dim light on the question of tribal membership of the Cherokee Nation and the other displaced Oklahoma tribes. Though “Lucas” has not yet applied, his father and many of his relatives still living in Oklahoma are members of the Cherokee Nation through their proven genealogical descent from ancestors on the Dawes Rolls. Yet, even though one of his chromosomes came from his European mother, there is really only one tiny speck of Native American DNA on the chromosome he inherited from his Cherokee father, which is far less than the average of 6 percent shown by the disenfranchised descendants of the Freedmen of Oklahoma.

Coupled with the almost complete absence of any Native American paternal or maternal ancestry among the Seaconke Wampanoag, as revealed by the Genographic Project, this only goes to show how incompetent DNA really is at assigning individuals to discrete categories. That is not the same as saying that race or ethnicity have nothing at all to do with genetics. After all, it is true that most African Americans do carry more African DNA than European Americans, and Ashkenazi Jews are more likely to be members of the clan of Katrine than the average native European, for example, but the correspondence is far too weak in individual cases for accurate assignment. However, the real problem here is not the basic genetics, which only seeks to describe underlying patterns of biological inheritance, but the human desire to create categories in the first place. Not wanting to wander into the well-trampled territory of the social and political ramifications of race and ethnicity any further than I already have, let me just quote one of my heroes, Arthur Mourant. He was among the tireless pioneers of blood grouping in the 1950s, when biology was first being proposed as a way of dividing up the world into discreet population units. He realized the fallacy when he wrote: “Rather does a study of blood groups show a heterogeneity in the proudest nation and support the view that the races of the present day are but temporary integrations in the constant process of . . . mixing that marks the history of every living species.”1 Substitute DNA for “blood groups” and modernize the literary style, and this could have been written today.

There is only one more observation to make in DNA USA, and it derives from the fascinating complexity of the human genome illustrated so well by the chromosome portraits of the sitters. This is most readily appreciated in the multicolored paintings of my African American volunteers, because here you can see most clearly how all of our bodies work on the intimate collaboration of DNA segments handed down by thousands if not millions of ancestors. The Native and European American genomes are equally complicated mixtures of ancestral contributions, but it is not so easy to see the individual components in the present color scheme.

To illustrate my point I have picked out 140 genes that help run eleven major body systems and shown their locations against the chromosome portrait of Mark Thompson, one of my African American volunteers. The composite portrait is the last in the gallery and I have put the detailed description of these genes in an appendix. These are only a tiny fraction of the total number of genes we need to keep going, but enough to convey the principle. In all of us they work equally from the two copies that we inherited, one from each of our parents. They have to cooperate properly, or we would simply not survive, as the example of severe inherited disease teaches us. So, whatever their own individual ancestry, whether African, European, or Native American, our genes must have found a way of working together. My pancreas functions on a combination of both African and European genes. Equally, “Rhett Butler,” a white man from the South, depends on the DNA inherited from an unknown African ancestor for his heart muscles to work properly. “Ilsa Lund”’s digestive system, and much else besides, runs on DNA from her African ancestors. “Atticus Finch” needs his Mohawk genes to make sure his red blood cells do their job well.

Unfortunately, in one respect, I did not get to paint the chromosome portrait of any self-confessed white supremacists or members of the Ku Klux Klan. Had they been from the South, then there would have been a very good chance that their portraits would have a few splashes of green. If that had been met with shock or denial, my next question would have been whether they would rather do without the African DNA. If the answer had been yes, I would point out that doing so would cause them to lose the use of their kidneys or heart muscles—or whatever the African DNA was doing for them. Would they go ahead and have these organs removed? I think not.

The essential genetic collaborations are even more obvious in the portraits of my African American volunteers. Mark Thompson’s insulin output is controlled by 100 percent European genes at the tip of chromosome 11, making his pancreas less “African” than mine. The same goes for his beta-globin genes, located right next door. They are both from European ancestors, which means that even though he is an African American he is extremely unlikely to be a carrier of sickle-cell anemia, which is caused by a mutation in this gene. I, on the other hand, could be a carrier, as this globin gene is located in the segment that I inherited from my African ancestor. This illustrates a relevant health-care issue. No doubt with the best of intentions, ethnicity is taken into account when deciding on diagnosis and treatment plans. Since I am easily classified as a white Caucasian, no one would ever suspect that I might be a carrier for sickle-cell anemia, which is an African disease, but I could well be.

During the Korean War in the early 1950s, American troops in the field were prescribed antimalarial drugs. About 10 percent of African American soldiers developed severe anemia after this treatment while European American soldiers only very rarely showed any side effects. It took a long time to pin down the cause, but it was eventually tracked to a deficiency in an enzyme with the shorthand G6PD, whose gene is carried on the X chromosome. As with sickle-cell anemia, carriers for the G6PD mutations have some resistance to malarial infection, and for this reason G6PD deficiency is more prevalent among people with ancestry from West Africa, where malaria is endemic. This was the first time anyone had noticed that there was a difference in the effects of pharmaceuticals between different racial groups, and it is regarded as the moment when the new field of pharmacogenetics was born. Since then there have been many more examples of severe side effects suffered by different ethnic or racial groups, which has had an influence on drug prescriptions and treatment plans.

Of these the most clinically relevant are the observed differences in the way people metabolize pharmaceuticals. Most drugs, and other toxins, are cleared from the body by the liver, using a series of proteins called P450 cytochromes. Many African Americans carry a version of the P450 gene located on chromosome 10 that is less active in clearing some widely used drugs, like beta-blockers, the blood thinner warfarin, and the anti-inflammatory drug diclofenac. As a consequence, African American patients are generally prescribed much lower doses of these drugs than are their European American counterparts. By now you will begin to see the dangers of the blanket application of this prescribing policy toward anyone classified as African American. If one or both of their P450 genes is actually European in origin, then the basis for prescribing the lower dose will be wrong. A quick scan through the chromosome portraits in the gallery reveals that of my nine African American volunteers, only three have both copies of their P450 gene from African ancestors, three have one European and one African copy, and the genes of the remaining three are completely European. Inversely, “Sugar Kane,” my European American volunteer from Florida, also carries an African version of P450 on her chromosome number 10, so even though she is unmistakably white she could well clear drugs more slowly than her physicians would expect using only her overall ethnic affiliation.

But it is not just the collaborations between African and European genes that are highlighted by the portraits. Another of my DNA volunteers, “Holly Golightly,” a distinguished African American biographer whom I met while she was on sabbatical in Oxford, was surprised when I told her that both copies of her lactase genes, located on chromosome 2, were inherited from Native American ancestors. She is lactose intolerant and had always put this down to her African background, whereas in fact her inability to break down lactose, which is found mainly in milk, is due to the poorly functioning lactase genes that she inherited from her Native American ancestors.

Possibly the most revealing feature of the chromosome portraits concerns the genes for the one trait that, more than any other has been used to define racial categories—that of color. All pigmentation in humans is due to just one basic substance, melanin. It alone is responsible for the vast range of skin and hair colors found in people from around the world. Melanin itself is a polymer derived from the amino acid tyrosine and is contained within pigmented cells, the melanocytes, in discrete granules. Basically, the more melanocytes and the more melanin in the granules, the darker the skin, eyes, and hair. Blue eyes are not blue because they contain a pigment but because, in the absence of melanin, light reflected from a layer in the iris is diffracted through the regularly spaced transparent collagen fibers in the cornea and gives the appearance of being blue; it is the same optical mechanism that imparts the vivid colors of a butterfly’s wing.

The genetic control of skin and hair pigmentation is orchestrated by eleven genes that we know about, though there may well be more. They each control different parts of the process of producing melanin granules and regulating the number of melanocytes. The paler end of the wide range of human pigmentation is probably a response to the reduced exposure to sunlight that some of our ancestors experienced when moving from Africa to higher latitudes. Some vital functions, like the synthesis of vitamin D and folic acid, depend on sunlight, so it makes sense that evolutionary natural selection would have promoted the survival of lighter-skinned individuals. When we look at the chromosome portraits, it is very clear that many of my African American volunteers, who count themselves as black, actually have a mixture of pigmentation genes from many different ancestries. To take just one example, the radio-talk-show host Mark Thompson. Of his eleven pigmentation genes, only two are of completely African origin, five have been inherited equally from European and African ancestors, two are an equal mix of African and Native American, and one has been inherited from exclusively European ancestors. That blend of origins is the direct result of the mixing of his chromosome segments in generations of his African, European, and Native American ancestors.

Since this process is more or less completely random, a vast number of combinations is possible in any African American. There will be individuals who actually have very little DNA from African ancestors, yet if these contributions include chromosome segments housing the pigmentation genes, then they will have typically dark coloring. Likewise there will be Americans whose DNA is almost all African in origin, yet if the pigmentation genes are not included in these segments and instead come from European ancestors, then their coloring will be white. Similarly, it would be entirely possible for a European American with only a small overall component of African DNA to be very dark skinned if these ancestral segments were to include the pigmentation genes. Our only Cherokee volunteer probably had a dark skin tone because the sole surviving segment of Native American DNA in his genome included one of the most influential of the pigmentation genes, located on chromosome 15.

As you leave the gallery, my hope is that you will come away with the feeling that you have glimpsed another world. A world that mocks the artificial divisions we have created for ourselves. A world made up of the corpuscles of DNA that each of us has inherited over millennia from our myriad ancestors, every one of them a resourceful survivor from earlier times. We are their privileged custodians in this world for a few short years, messengers through time to generations not yet born. Let us enjoy this honor while we may.