|
|
re:大脑：语言化石埋在你身体的每一个细胞中...
大脑：语言化石埋在你身体的每一个细胞中
http://article.yeeyan.org/view/202015/230433
一个英国家族出现了奇怪的语言缺陷，这一缺陷让语言学家们发现了FOXP2基因，从此找到人类祖先习得语言的秘密。
作者：卡尔·齐默
本文刊登在2011年10月的发现杂志上，网络版发表日期：2011年10月17日
对于人类的进化史来说，没什么东西比语言的出现更为重要，正是因为我们的祖先可以通过语言互相交流，人类之间的互助合作才显得更加强大有力。然而遗憾的是，语法却无法通过化石的形式留存给后世。在现代社会中，我们更是处处被文字包围着——口头语、书面语、手势语、还有写在纸上的文本——它们成了人类区别于其他生物的基本特征。可是，我们却没法在埃塞俄比亚的山坡上挖到一块化石，然后指着一块人骨化石，称“这就是语言的起源。”（译者按：在埃塞俄比亚发现了最古老的人类化石）
因为缺乏强有力的证据，过去的学者只能对语言的起源进行大胆的假设。有人说，语言始于痛苦的喊叫，后来才慢慢形成清晰的单词。还有人认为语言起源于音乐，或者源于人们对兽类或鸟类声音的模仿。1866年，法国语言学协会终于对这些天马行空的揣测忍无可忍，禁止任何对语言起源的交流。而英国的语言学家们在这件事情上也持相同的观点。1873年，伦敦语言学协会宣布：语言学家们“应该致力于探寻某一日常语言的历史发展过程，而不应对所有语言的起源做那些吃力不讨好的无端揣测——这些揣测的文字最终都只能扔进废纸篓里。”
一个世纪过去了，语言学家们终于改变了初衷——语言起源一事再次被严肃地提起。这种改变来源于他们开始从语言的深层结构上研究语言本身。麻省理工的语言学家诺姆·乔姆斯基认为：儿童之所以可以轻松地习得语言，一定有其生物学基础。在这一观点的基础上，乔姆斯基的某些同事提出了他们的主张——语言的进化就像眼睛和翅膀一样，也是自然选择的结果。果真如此的话，通过观察与我们亲缘关系最近的灵长类动物之间的沟通交流，就可能从中发现某些线索，证明人类语言到底是怎样从咕哝有声或者打手势进化而来的。
（这篇文章没翻译完，下面是英文的）
This line of thinking raised an exciting possibility: Perhaps language left a fossil record after all—not in buried bones, but in our DNA. Yet for years biologists could not find a single gene involved in language.
Ten years ago, that finally changed. In 2001 a team of British scientists announced the discovery of a gene, called FOXP2, that seems to be essential for language. FOXP2 came to light through the study of a family that had unusual difficulties with words. The KE family—so called in scientific papers for privacy reasons—lived in West London and included nine siblings, some of whom attended the same special speech and language school. Psychologists at the school discovered that four of the children struggled with language in a similar way. The meaning of sentences sometimes confused them: They might misinterpret “The girl is chased by the horse” to mean “The girl is chasing the horse.” They also had trouble speaking—dropping some sounds off the beginning of words, for example, so that they would say “able” when they meant “table.”
In 1987 the school headmistress referred the case to the Institute of Child Health at University College London. There, neurologists found that some of the children’s cousins had the same language troubles, as did some of the parents. Geneticists traced the condition to a grandmother and deduced that she probably carried a rare mutation that she had passed along. The mutation did not alter intelligence or psychological well-being; the KE family was normal in those regards. Its effects were limited to language—but within that narrow sphere, its effects were profound.
The family then came to the attention of geneticists at Oxford, who began a dogged search for the gene that caused these problems. They compared the DNA of family members, looking for distinctive markers shared only among the ones who had trouble with language. Among those with the language deficit, they found shared markers in a single region of chromosome 7. Years later, the scientists received a vital new clue when the same kind of language disorder was identified in an unrelated 5-year-old boy. He had experienced a particularly dramatic mutation, in which a piece of chromosome 5 had been swapped with a piece of chromosome 7. One end of the boy’s swapped DNA lodged itself in the same region that the Oxford team had identified in the West London family, right in the middle of the FOXP2 gene.
The Oxford researchers turned back from the boy to the KE family and, using the additional information, discovered that those members with language troubles shared a mutation in FOXP2 as well. Their mutation was far more subtle, however. Their trouble with language had been caused by the change of a single nucleotide of DNA—just one letter in the genetic sequence.
All land vertebrates carry a version of the FOXP2 gene, so some of the Oxford researchers then teamed up with colleagues from the Max Planck Institute for Evolutionary Anthropology in Germany to analyze what is unique about the variant in humans and to track how the gene had evolved in our ancestors. They determined that after the gene arose, more than 300 million years ago, it barely changed in most branches of vertebrate evolution to the present day. In the human branch, however, two amino acids in the protein produced by the FOXP2 gene changed notably over the course of just a few million years. The scientists concluded that FOXP2 experienced a fast pulse of natural selection in our lineage, a development possibly related to the emergence of language.
The FOXP2 gene also is associated with vocal learning in young
songbirds, which produce higher levels of protein when they learn new songs. If FOXP2 is impaired, they make singing mistakes.
Several groups are now hard at work gleaning more details about the relationship between FOXP2 and language. Cognitive neuroscientist Frederique Liegeois of University College London is using fMRI scans to compare the brain activity of members of the KE family who have a mutated copy of FOXP2 with those who have a normal version. The most striking difference, Liegeois recently reported, arises when family members are asked to repeat a set of nonsense words, something most adults can do without trouble. Those with the mutation do badly at the task. They also have low levels of activity in several regions of the brain, especially the basal ganglia, a key hub for learning muscle movements. That makes sense, since one of the hardest aspects of speech is learning how to make the necessary rapid movements of the lips, tongue, and vocal cords.
Other scientists are probing the FOXP2 gene further by studying the protein it produces, known as FOXP2. The protein seems to be especially active while human embryos are developing. Simon Fisher—one of the original Oxford geneticists, now at the Max Planck Institute for Psycholinguistics in the Netherlands—has found that the gene switches on in neurons within certain regions of the brain, including the basal ganglia. The FOXP2 protein then latches onto other genes in developing neurons and switches them on or off as well. By orchestrating dozens of genes, FOXP2 appears to oversee the growth of new branches on the neurons, bringing about a level of complexity likely to facilitate language.
Humans are not the only species to benefit from FOXP2. Researchers have shown that the gene is associated with vocal learning in young songbirds, which produce higher levels of FOXP2 protein when they need to learn new songs. If their version of FOXP2 is impaired, they make singing mistakes. Other vocal-learning species, such as whales, bats, elephants, and seals, may also rely on the gene. To probe this connection, geneticist Wolfgang Enard of the Max Planck Institute for Evolutionary Anthropology engineered mice by replacing their FOXP2 gene with the human one. The mice did not start reciting poetry, but they did display some subtle changes. Instead of producing a high squeak, for example, the engineered mice produced lower sounds. Bigger changes took place within the animals’ brains. Enard found that in the basal ganglia and connected regions involved in learning, the human version of FOXP2 caused some neurons to develop longer branches than those found in normal mice. Around the same time, Fisher and his team engineered mice so that one copy of their FOXP2 gene carried the same mutation as that found in the KE family. In subsequent tests, the mice with the mutation did a worse job than normal mice at learning new motor skills.
These findings hint at what happened to FOXP2 in our ancestors. It may have started out hundreds of millions of years ago as a gene that helped regulate the learning of body movements, such as those involved in running, calling, and biting. Later mutations in the gene spurred more neural growth in certain areas of the brain, including the basal ganglia, creating the connections essential for learning and mastering complicated sounds and, eventually, full-blown language.
FOXP2 didn’t give us language all on its own. In our brains, it acts more like a foreman, handing out instructions to at least 84 target genes in the developing basal ganglia. Even this full crew of genes explains language only in part, because the ability to form words is just the beginning. Then comes the higher level of complexity: combining words according to rules of grammar to give them meaning.
Language is nearly endless in its forms. So the search for its behavioral fossils—genes associated with grammar and syntax—should keep scientists busy for decades to come.
Carl Zimmer is an award-winning biology writer and author of The Tangled Bank: An
Introduction to Evolution. He blogs at The Loom.
|
|
IP卡
狗仔卡
发表于 2011-11-7 15:51:32
显身卡
