译者 Bingy
The Brain － The Language Fossils Buried in Every Cell of Your Body
大脑：你身体里每个细胞都埋藏着语言的化石
by Carl Zimmer
作者：卡尔 齐默
From the October 2011 issue; published online October 17, 2011
发表于《探索发现杂志》2011年10月刊，2011年10月17日网上发行
It is a shame that grammar leaves no fossils behind. Few things have been more important to our evolutionary history than language. Because our ancestors could talk to each other, they became a powerfully cooperative species. In modern society we are so submerged in words—spoken, written, signed, and texted—that they seem inseparable from human identity. And yet we cannot excavate some fossil from an Ethiopian hillside, point to a bone, and declare, “This is where language began.”
语法没有给我们留下任何化石证据实在是天大的遗憾。在我们的进化历史当中，很少有其他因素能与语言的重要性相提并论。我们的祖先能够相互交谈，因而才成为有强大合作能力的物种。现代社会中的我们更是被淹没在语词之中——说出来的、写下来的、签在纸上的和敲打在短信里面的——他们几乎已经与人类的身份密不可分。然而我们却无法从埃塞俄比亚的山坡上挖出几块化石，指着其中一块骨头宣布。“这就是语言的诞生地。”
Lacking hard evidence, scholars of the past speculated broadly about the origin of language. Some claimed that it started out as cries of pain, which gradually crystallized into distinct words. Others traced it back to music, to the imitation of animal grunts, or to birdsong. In 1866 the Linguistic Society of Paris got so exasperated by these unmoored musings that it banned all communication on the origin of language. Its English counterpart felt the same way. In 1873 the president of the Philological Society of London declared that linguists “shall do more by tracing the historical growth of one single work-a-day tongue, than by filling wastepaper baskets with reams of paper covered with speculations on the origin of all tongues.”
由于缺少可信的证据，对于语言的起源，以往的学者往往只能推测。有的学者宣称语言最早始于疼痛导致的喊叫，然后逐渐形成可辨别的词汇。还有的人把语言起源与音乐、模仿鸟和动物的叫声等联系起来。1866年，巴黎语言学会对这些漫无边际的胡思乱想忍无可忍，因此全面禁止了有关语言起源的学术交流。他们的英国同行也有同感。1873年伦敦文献学会宣布语言学研究者们“应更多地追溯某一种语言的历史沿革，而不是在推测所有语言的起源这类事上面浪费纸张。”
A century passed before linguists had a serious change of heart. The change came as they began to look at the deep structure of language itself. MIT linguist Noam Chomsky asserted that the way children acquire language is so effortless that it must have a biological foundation. Building on this idea, some of his colleagues argued that language is an adaptation shaped by natural selection, just like eyes and wings. If so, it should be possible to find clues about how human language evolved from grunts or gestures by observing the communication of our close primate relatives.
从那时起过了一个世纪，语言学家们才开始转变思想。他们开始检视语言本身的深层次结构。麻省理工的语言学家诺曼 乔姆斯基断言，由于儿童学习语言的方式如此轻松，因此必定有其生物基础。从这个观点出发，他的同僚们也主张语言是由于自然选择而形成的适应结果，就像眼睛和翅膀一样。如果属实，那就应该有可能找到从观察模仿我们的灵长类近亲用叫声或手势交流而逐渐进化到人类语言过程的痕迹。
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.
这种思路展现了一种激动人心的可能性：语言可能留下了化石纪录——不是埋在地下的骨头，而是在我们的DNA当中。然而，生物学家多年来都无法找到哪怕一条和语言有关的基因。
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.”
十年前，这种局面终于被打破了。2001年，一组英国科学家宣布他们发现了代号为FOXP2的基因，该基因似乎对语言至关重要。FOXP2是通过对一个患有罕见语言障碍的家庭的研究而发现的。为了保护隐私，论文中称这家庭为“KE”，他们居住在伦敦西区，包括九名表亲，有些还在同一所特殊语言学校上课。该校的心理学家发现了四名患有相似语言困难的儿童。他们往往会混淆句子的意义：如他们会把“小女孩被马追”错误地理解成“小女孩追马”。他们在表达上也有问题，常常丢掉一些词汇开头的音素，例如他们会说“能（able）”，但实际上想说的是“桌子（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.
1987年，学校校长将这些儿童的案例提交至伦敦大学学院儿童健康研究所。在那里，神经学家发现这些儿童的表亲及父母也患有同样的语言困难。遗传学家最终将这种现象追溯到一位祖母身上，推断她身上很可能发生了某种罕见的基因突变，并将其传给了她的后代。这种突变对智能和心理健康没有影响，KE家庭在这些方面完全正常。它的效果仅表现在语言上，不过在这个很小的范围内，其影响是深刻的。
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.
随后，牛津大学的遗传学家们也开始注意到了这个家庭，并对导致该问题的基因展开了不懈的搜寻。研究者将家庭成员的DNA进行比对，寻找仅仅在患有语言障碍的家庭成员身上才带有的明确标记。在这些家庭成员的第七条染色体同一区域内，发现了他们共有的标记。多年以后，又有一个和KE家庭没有血缘关系的五岁男孩被诊断出了同样的语言障碍，在他身上科学家们又得到了一条至关重要的新线索。这个男孩经历了一次尤其剧烈的突变，他的第五条和第七条染色体各有一个片段互相交换了位置。被交换的片段一端正好镶嵌在牛津大学人员在伦敦西区那个家庭中发现的标记的位置上，就在FOXP2基因的中间。
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.
从这个男孩身上，牛津大学的科学家又转回到KE家庭，利用获得的新线索，他们发现那些有语言障碍的家庭成员在FOXP2基因上也都有相同的突变，只是相对较不明显。他们的语言问题仅仅是因为DNA中一个核苷酸发生了改变，也就是说基因序列中有一个字母被改写了。
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.
所有陆生脊椎动物都带有某种形式的FOXP2基因，因此牛津大学的学者们随即和德国马克斯 普朗克进化人类学研究所进行了合作，对该基因人类版本的特殊性进行分析，并跟踪它在人类祖先身上的进化历程。他们认定，FOXP2基因产生于三亿年前，此后直到今天，绝大多数脊椎动物身上的这个基因几乎没有改变过。然而在人类这个分支中，FOXP2基因产生的蛋白质中有两个氨基酸在一两百万年内发生了明显的变化。科学家的结论是FOXP2基因在我们这条血脉的自然选择过程中发生了一次快进，这种发展可能与语言的出现有关。
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.
目前有数个团队正在努力寻找关于FOXP2基因和语言之间的联系的更多细节。伦敦大学学院的认知神经学家弗雷德里克 列日瓦使用功能性核磁共振（fMRI）对KE家庭中FOXP2基因产生突变的成员和其他家庭成员的大脑活动进行比对。列日瓦最近的报告称，两组之间最显著的不同在于当他们被要求重复一组没有任何意义的词语时（这件事大多数成年人都没有任何困难），那些产生了基因突变的家庭成员表现非常糟，同时他们的大脑活动水平在若干区域内也非常低，尤其在基底神经节上，而基底神经节是学习肌肉运动的关键环节。这种发现是说得通的，学习语言当中最困难的部分就是如何使用嘴唇、舌头和声带作出相应的迅速运动。
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.
别的科学家们通过研究FOXP2基因产生的蛋白质来对该基因进行深入探索，这些蛋白质也叫做FOXP2。这写蛋白质在人类胚胎发育的时候似乎尤其活跃。西蒙 费舍尔是牛津大学最初参加该项研究的遗传学家之一，现在供职与荷兰的马克思普朗克语言心理学研究院。他发现了在如基底神经节的大脑某些区域内的神经元中，该基因是打开的。FOXP2蛋白质随即附着在其他用于发展神经元的基因上，并同样控制它们的开启和关闭。通过如此指挥数十个基因，FOXP2仿佛在监管新神经元突触的生长，提供发展语言所需的复杂功能。
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.
人类并不是唯一受益于FOXP2基因的物种。研究者们已经发现该基因还和鸣禽幼雏学习发声有关，当幼鸟们学习歌唱时，该基因会产生更多的蛋白质。如果FOXP2基因受损，它们就会唱错。其他学习发声的物种，如鲸、蝙蝠、象和海豹等，可能也仰赖该基因的作用。为了探索这种联系。马克思普朗克进化人类学研究所的遗传学家沃尔夫冈 恩纳德培养了一种发音更低沉的老鼠。动物的大脑中发生的变化更为显著。恩纳德发现在基底神经节和周围与学习有关的区域中，人类FOXP2基因导致有些神经元生长出比普通老鼠更长的突触。与此同时，费舍尔和他的团队也培养了在FOXP2基因中一种携带和KE家庭同样突变的老鼠。在随后的试验中，这些携带突变的老鼠在学习新动作上远远落后于普通老鼠。
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.
这些发现都在暗示我们祖先身上FOXP2基因所发生的变化。也许在数亿年前，一个帮助身体学习诸如奔跑、喊叫和撕咬之类动作的基因开始了变化。随后该基因发生的突变引起大脑的基底神经节等区域中更多的神经生长，创造了那些对学习和掌握复杂声音至关重要的连结，最终产生了真正的语言。
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.
我们的语言并不全是拜FOXP2所赐。在我们的大脑中，它就像一个指挥，向基底神经节中其他至少84个基因下达指令。就算这些基因加在一起，也不过能够部分解释我们的语言能力，因为形成词汇不过是个开始。接下来还需要更高的复杂处理能力：根据语法规则组织词汇，赋予它们意义。
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.
语言表现形式是无穷无尽的。因而对与语言行为的化石证据——即和语法句法有关的基因——的搜寻，足够科学家们忙上几十年了。
Carl Zimmer is an award-winning biology writer and author of The Tangled Bank: An Introduction to Evolution. He blogs at The Loom.
（卡尔 齐默是一名获奖的生物科普作家）
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