Those children would have fascinated Buffon. In his search for an explanation for albinism, grasping at a theory of inheritance that did not yet exist, he was keen to know what the offspring of a union between an albino and someone with normal pigmentation would be. He thought they might be piebald. In the Histoire naturelle he gives another lithograph. This one is of a girl, perhaps four years of age, standing amid a clutter of exotic artefacts: a parasol, axes, a blanket and a feathered headdress. A small parrot, a household pet, perches upon her hand suspended in mid-air. The girl has a two-tone body: a mosaic of black and white.
Buffon never met the child, knew little about her origins, and described her entirely from a picture. Painted in Columbia by an unknown artist around 1740, the portrait was dispatched to Europe on a Spanish vessel which was promptly seized by the West Indies squadron of the Royal Navy. Now a trophy of war, the picture was taken to Carolina where it was copied at least twice. One of these copies, or perhaps the original, was sent to London, but this ship was plundered as well – it was the French navy’s turn – and the painting was placed in the hands of the Burgomaster of Dunkirk, a M. Taverne, who sent it to Buffon. And so the War of the Spanish Succession brought Marie Sabina, the piebald child, to the eyes of Europe’s greatest naturalist.
Buffon was enchanted. His copy of the portrait, which is now lost, bore the following inscription:
The True
Picture of Marie-
Sabina who was born
Oct 12 1736 at Matuna a
Plantation belonging to
the Jesuits in the City of
Cartegena in America of
Two Negro Slaves named
Martianiano and Patrona.
In a letter that he sent with the portrait Taverne wrote: ‘In spite of the legend, I think that the child is the issue of a union between a white and a négresse, and that it was to preserve the honour of both the mother and the Society [of Jesus] whose slave she was, that it states that both the parents were black.’ Buffon replied that although he initially thought that Taverne’s explanation might be true, upon reflection he doubted that it could be. There were thousands, millions, of people of mixed black and white blood, and they all appeared to be uniform brown in colour. Perhaps, he continued, the child was the progeny of a black and an albino – one of those anomalous Blafards. And that is all we know about Marie Sabina, bar a brief mention by the Jesuit geographer and ethnographer José Gumilla, who in his Orinoco illustrado, y defendido, historia natural y geographica de este gran rio (Madrid, 1745) records that he encountered her as an infant in a plantation hospital, told her mother (who was recuperating) to beware that others did not cast an evil eye upon her daughter, and concluded that the child’s peculiar appearance could almost certainly be blamed on the dog, a household pet, which had the misfortune to be spotted as well.
Buffon’s hypothesis – that piebald children were the progeny of albinos and blacks – ran for nearly two hundred years. It was certainly a more reasonable theory than Gumilla’s spotted dog, yet its longevity remains surprising, since in that time at least four other piebald children emerged from the Caribbean onto the pages of learned journals, and not one had an albino parent. Besides Marie Sabina, there were John Richardson Primrose Bobey (b.1774, Jamaica), Magdeleine (b.1783, St Lucia), George Alexander Gratton (b.1808, St Vincent), and Lisbey (b.1905, Honduras). Each child was celebrated in its day. Portraits of Marie Sabina now hang in Williamsburg, Virginia, and at the Hunterian Museum in London; Magdeleine has a statue at Harvard University; and in Marlow, Surrey, George Gratton has a grave with the epitaph ‘Know that there lies beneath this humble stone/a child of colour haply not thine own.’
The most recent of these Caribbean piebalds, Lisbey, featured in an article written by the British geneticist Karl Pearson in 1913. Like Buffon, Pearson thought that piebalding had something to do with albinism. He does not suggest that the child’s mother had an affair with an albino – a photograph of the family shows a lace-clad matriarch of seemingly imperturbable moral rectitude. Instead he questions Lisbey’s ancestry, postulating the existence of an albino forebear. Pearson’s hypothesis was a bit more complex than this, for he also proposed that an albino ancestor will only cause piebalding when one of the parents is particularly dark – and Lisbey’s father was, in Pearson’s words, ‘a coal black negro’. It is a convoluted explanation and one that is difficult to understand from a modern point of view. We now know that piebalding has nothing to do with albinism but is instead caused by dominant mutations in an altogether different set of genes, and that these mutations can occur in people of any colour – not to mention horses, cats, and a strain of mouse called ‘splotch’. They are no less fascinating to us than Marie Sabina was to Buffon. Among other things, they tell us about the strange origin of the cells that colour our skins.
Melanocytes spend their lives in the skin, but they are immigrants there. Where most of the skin is ectoderm, melanocytes are the products of a tissue called the neural crest. At about day 28 after conception, neural crest cells flow out of the newly formed dorsal nerve cord and pour themselves around the foetal head to make the face. But some neural crest cells travel much further than this. As a river fans out over its delta, streams of neural crest cells course down from the escarpment of the dorsal nerve cord and penetrate to the embryo’s farthest reaches. In one part of the body they form nerves, in another muscles, yet elsewhere they invade developing glands. And some become melanocytes which, early in foetal life, invade the lower layers of the skin where they settle down to produce pigments. Neural crest cells make our faces, and they also lend them colour.
Molecular devices are required to make a naive neural crest cell form a melanocyte rather than some other kind of cell, and also to guide the melanocytes to their final destinations. Mutations in at least five distinct genes cause piebaldism, and each of them disables one or more of these devices, so causing patches of skin that are devoid of melanocytes and therefore perfectly white. Some piebalds have only a white forelock, some have bodies covered in patches, and some have eyes of different colour. Yet others have more serious disorders. A few piebald infants have a debilitating intestinal condition known as ‘megacolon’ – a lower intestine that is swollen with massive constipation caused by the absence of gut nerves that drive defecation. These nerves too have their origin in the neural crest. Piebald children are also prone to deafness, for it seems that melanocytes serve some critical function in the inner ear.
DINKA VS. DUTCHMAN
Guinea pigs, dogs, cats and cattle may have been bred for variety of colour, but only humans come naturally in so many different shades. What gives us our skin colours? It is a curious thing, but for all that geneticists have learned about the causes of abnormal pigmentation, they have yet to give an account of the genes responsible for the difference in skin colour between, say, a Dinka and a Dutchman.
Why is this? In part it is due to the sheer difficulty of the problem. Geneticists agree that more than one gene makes the difference between naturally dark and fair skin (were it only one gene, we would know it by now), but beyond that the guesses range between two and six, interacting in complex combinations to give any particular shade of pink, tan, brown or black. This makes things difficult. When many genes, each of which has many variants, combine to affect some property of the human body, the molecular identification of those genes becomes a challenging exercise in applied statistics. When the property in question is a disease – heart disease or non-insulin-dependent diabetes – geneticists have embraced the challenge with a will. They have been more cautious about studying skin colour.