A remarkable new line of inquiry bearing on the origins of language has recently been opened up by the human genome project. This is the discovery of a gene that is intimately involved in many of the finer aspects of language. The gene, with the odd name of FOXP2, shows telltale signs of having changed significantly in humans but not in chimps, exactly as would be expected for a gene serving some new faculty that had emerged only in the human lineage. And, through the ability of genetics to reach back into the distant past, the emergence of the new gene can be dated, though at present only very roughly. FOXP2 came to light through the discovery by Jane Hurst, an English geneticist, of an unusual London family whose existence she reported in 1990. The family consists of three generations. Of the 37 members old enough to be tested, 15 have a severe language deficit. Their speech is hard to understand, and they themselves have difficulty comprehending the speech of others. If asked to repeat a phrase like "pattaca pattaca pattaca," they will stumble over each word as if it were entirely new. They have difficulty with a standard test of the ability to form past tenses of verbs ("Every day I wash my clothes, yesterday
I_my clothes"; four-year-olds will say "washed" as soon as they get the idea). They have problems in writing as well as speaking. The affected members of the family have been given intensive speech training but mostly hold jobs where not much talking is required. "Their speech is difficult to understand, particularly over the telephone, or if the context is not known. In a group of family members it is hard for you to pick up the pieces of the conversation, which is difficult to follow because many of the words are not correctly pronounced," says Faraneh
Vargha-Khadem of the Institute of Child Health in London.55 Some of the first linguists to study the affected family members believed their problem was specific to grammar but Vargha-Khadem has shown that it is considerably wider. Affected members have trouble in articulation, and the muscles of their lower face, particularly the upper lip, are relatively immobile. It could be argued that their defect stemmed from some general malfunction in the brain, which was not specific to language. But the IQ scores of the affected members, though low, fell in a range (59 to 91) that overlapped with that of the unaffected members (84 to 119).^^ The core deficit, Vargha-Khadem concluded, is "one that affects the rapid and precise coordination of orofacial [mouth and face] movements, including those required for the sequential articulation of speech sounds."57
The affected members of the KE family, as it is known, have each inherited a single defective gene from their grandmother. They provide the results of an experiment that no one would even contemplate doing in humans, but which nature has performed nonetheless—what happens if you disable a critical speech gene? And the one disabled in the KE family seems to operate at such a sophisticated level that it looks as if it were one of the last genes to be put in place as the faculty of language was perfected.
In 1998 a team of geneticists at Oxford University in England set out to identify the defective gene by analyzing the genome of KE family members. Their method was to look for segments of DNA that the affected members shared and the unaffected lacked. The Oxford team soon narrowed the cause of the problem to a region on chromosome 7, the seventh of the 23 pairs of chromosomes in which the human genome is packaged. Within this region lay more than 70 genes, and it seemed that it would take several years to study each gene and see which one was responsible. But Hurst then turned up a new patient with the same rare set of symptoms. The patient, a boy, had a break in his chromosome 7 that disrupted one of the genes in the section the Oxford team was studying. It was an easy task to identify which of the new patient's genes had been broken. It was a gene
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