Evolution of a single gene linked to language

[Freeman]

人类语言功能关键基因

为什么人能说话而其生物学近亲黑猩猩却不能？英国《自然》杂志今天2009－11－12刊登研究报告说，答案可能就在基因FOXP2上，这个基因的人类
版本与黑猩猩版本仅有两点小小的不同，但却因此赋予人类独特的语言能力。

http://www.nature.com/news/2009/091111/full/news.2009.1079.html

Mutations in the FOXP2 gene could help explain why humans can speak
but chimps can't.

Kerri Smith


Changes to the sequence of one gene may help to explain why humans
talk but chimps don't.mlorenzphotography/ GettyTwo tiny changes in the
sequence of one gene could have helped install the mechanisms of
speech and language in humans.

In 2001, a gene called FOXP2 was found to underlie a rare inherited
speech and language disorder1. It encodes a transcription factor
called FOXP2, a protein 'dimmer-switch' that binds to DNA and helps to
determine to what extent other genes are expressed as proteins.

Experiments have now revealed that the human version of FOXP2, which
has two different amino acids compared with the version carried by
chimps, has differing effects on genes in the brains of the two
species. These differences could affect how the brain develops, and so
explain why only humans are capable of language.

To find out whether these changes in FOXP2 had a biological function,
a team led by Daniel Geschwind of the University of California, Los
Angeles, inserted the two versions into human brain cells and looked
at expression of the genes that the protein regulates. They found that
the human version increased the expression of 61 genes and decreased
the expression of 51 genes compared with the chimp version of the
protein. To double-check that the same was happening in real brains,
they looked at the expression of these genes in human and chimp brain
tissue and found similar expression levels as in the cells. Their
study is published in Nature2.

Master switch?
Many of the genes looked at by the team are known to have roles in
brain development and function, firming up the central place of FOXP2
in the brain's language and speech networks. They also affect soft-
tissue formation and development, linking FOXP2 to the physical side
of speech and articulation.

"I'm not a person who necessarily believes that one gene is going to
tell us everything, but this was really quite remarkable and does
place FOXP2 in a relatively central position," says Geschwind.

The study also lends weight to the idea that language didn't evolve
from scratch. It "depended on the retuning of genetic pathways present
in non-verbal ancestors, rather than the appearance of completely
novel mechanisms", says Simon Fisher of the Wellcome Trust Centre for
Human Genetics in Oxford, UK, and part of the team that discovered the
gene and first linked it to language.

Whether FOXP2 is the main driver of the evolution of language in
humans, or just a cog in the wheel, remains unclear, says Fisher. "It
is worth remembering that a large number of genetic differences
distinguish the brains of these two species, not just the
substitutions in FOXP2," he adds.

Differences in the cells or even in the animals used for the analysis
could also skew the picture. "The results could depend on particular
cell-line samples or particular humans or chimps," says Wolfgang
Enard, who studies the evolutionary history of FOXP2 at the Max Planck
Institute for Evolutionary Anthropology in Leipzig, Germany.

Geschwind and his team now plan to dig deeper into the genes that
FOXP2 regulates and find out whether these too are different in humans
from in chimps. "It's plausible that since language is so important,
that not only FOXP2 but many of its targets might be under selection,"
he says.

The team would like to know where these genes are expressed in the
brain, and what kind of brain cells they are most active in. Their
results could even throw up new candidates for genetic screening
programmes aimed at identifying language impairments, Geshwind says.