Read Mutants Online

Authors: Armand Marie Leroi

Mutants (29 page)

What made Geneviève white? Buffon was certain that Linnaeus’
Homo troglodytes
was just an ape. As for the
Blafards, Kakurlakos
and
Chacrelats
, these were merely descriptions of anomalously depigmented people living amid an otherwise dark-skinned population. One in ten children born in the Caribbean islands, he was told, was an albino. Geneviève’s parents were black, as were her siblings; whatever the cause of her whiteness it could not be contagious or even racial. Though he failed to solve the problem of albinism, when compared to the
fantasies of Linnaeus, Buffon left it immeasurably clearer. He also commissioned a lithograph of Geneviève, which shows her standing amid tropical fruit, quite naked and snow-white, as if in a photographic negative, smiling gently, perhaps at the absurdity of scientists.

O
CULOCUTANEOUS ALBINISM TYPE II
.
GENEVIèVE
. F
ROM
G
EORGE
L
ECLERC
B
UFFON
1777
Histoire naturelle générale et particulière.

THE PALETTE

We are a polychrome species. Yet the palette of human colour has only two pigments on it. One, eumelanin, is responsible for the darker shades in our skin, hair and eyes, the browns and the blacks; the other, phaeomelanin, for the fairer shades, the blonds and reds. As a painter mixes three primary colours to get all others, so too the various shades of our skins are given by the mix of these pigments.

Blacks have lots of eumelanin; redheads have lots of phaeomelanin; blonds have little of either. Albinos have no skin pigments at all. The pigments themselves are made in cells called melanocytes that are found within the top layers of the skin, the epidermis. These melanocytes package pigments into sub-cellular structures called melanosomes which they then transfer to the skin cells immediately above them, giving them colour. Mutations in several genes cause albinism. The most common disables one of the enzymes that melanocytes use to make pigment. In such cases even the eyes are devoid of pigment, and their redness comes from the retina’s blood vessels. The absence of pigment makes albinos sensitive to light and they often squint – hence the photophobia and slanted eyes of the
Kakurlakos
and
Blafards
. But some
albinos have at least some pigment in their eyes, and in these cases the defect lies in a protein that is called, somewhat enigmatically, ‘P’, used in the packaging and transport of melanosomes. Geneviève’s eyes were grey, not red, and it is almost certain that both copies of her P gene were defective. We can even guess what the mutation was. The most common cause of albinism in Africa is homozygosity for a 2.7 kilobase-pair deletion in the P gene. The same mutation is found in the Caribbean and among blacks in the United States as well, carried there by the slave trade.

There are no tribes, races or nations of albinos anywhere in the world; however, Pliny’s Leucaethopes are not entirely without foundation. About 1 in 36,000 Europeans is born albino, and 1 in 10,000 Africans. But the number jumps to 1 in 4500 among the Zulu and 1 in 1100 among the Ibo of Nigeria, and in very local populations the frequency can become even higher. In 1871,
en route
to his encounter with the Aka pygmies, George Schweinfurth came across some.

There is one special characteristic that is quite peculiar to the Monbuttos. To judge from the hundreds who paid visits of curiosity to my tent, and from the thousands whom I saw during my three weeks sojourn with Munza, I should say that at least
5
per cent of the population have light hair. This was always of the closely-frizzled negro type, and was always associated with the lightest skin that I had seen since leaving lower Egypt…All the individuals who had this light hair and complexion had a sickly expression about the eyes and presented many signs of pronounced albinism.

That albinism can be so common is a bit surprising. African albinos have, by any account, a hard time of it. Not only do they often suffer social discrimination and have difficulty finding marriage partners, but for want of pigment they cannot work for any length of time outdoors, and they are also prone to melanomas, a particularly destructive variety of skin cancer. These selective disadvantages should act to keep albino genes, and hence albinos, rare. Some geneticists have suggested that one reason for the high frequency (1 in 200) of albinism among the Hopi Indians of Arizona is that albino men, excused from working in the fields, stay at home and therefore dally among the women. But the evidence for this seems to rest on the charms of one old Hopi gentleman who was reputed to have fathered more than a dozen illicit children.

PIEBALDS

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.

P
IEBALDING
. M
ARIE
S
ABINA
, C
OLUMBIA
1749. F
ROM
G
EORGE
L
ECLERC
B
UFFON
1777
Histoire naturelle générale et particulière.

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.

P
IEBALDING
. L
ISBEY
, H
ONDURAS
1912. F
ROM
K
ARL
P
EARSON ET AL
. 1913
A monograph on albinism in man
.

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.

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