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Fri, 18 Nov 2011 21:07:41 -0500
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'Language Gene' Speeds Learning

     Mouse study suggests that mutation to FOXP2 gene
     may have helped humans learn the muscle movements
     for speech.

Ewen Callaway
18 November 2011
http://www.nature.com/news/language-gene-speeds-learning-1.9395

A mutation that appeared more than half a million years
ago may have helped humans learn the complex muscle
movements that are critical to speech and language.

The claim stems from the finding that mice genetically
engineered to produce the human form of the gene, called
FOXP2, learn more quickly than their normal
counterparts.

The work was presented by Christiane Schreiweis, a
neuroscientist at the Max Planck Institute (MPI) for
Evolutionary Anthropology in Leipzig, Germany, at the
Society for Neuroscience meeting this week in Washington
DC this week.

Scientists discovered FOXP2 in the 1990s by studying a
British family known as 'KE' in which three generations
suffered from severe speech and language problems1.
Those with language problems were found to share an
inherited mutation that inactivates one copy of FOXP2.

Most vertebrates have nearly identical versions of the
gene, which is involved in the development of brain
circuits important for the learning of movement. The
human version of FOXP2, the protein encoded by the gene,
differs from that of chimpanzees at two amino acids,
hinting that changes to the human form may have had a
hand in the evolution of language2.

A team led by Schreiweis' colleague Svante Pääbo
discovered that the gene is identical in modern humans
(Homo sapiens) and Neanderthals (Homo neanderthalensis),
suggesting that the mutation appeared before these two
human lineages diverged around 500,000 years ago3.

Altered squeaks
A few years ago, researchers at the MPI Leipzig
engineered mice to make the human FOXP2 protein4. The
`humanized' mice were less intrepid explorers and, when
separated from their mothers, pups produced altered
ultrasonic squeaks compared to pups with the mouse
version of FOXP2.

Their brains, compared with those of normal mice,
contained neurons with more and longer dendrites - the
tendrils that help neurons communicate with each other.
Another difference was that cells in a brain region
called the basal ganglia were quicker to become
unresponsive after repeated electrical stimulation, a
trait called `long-term depression' that is implicated
in learning and memory.

At the neuroscience meeting, Schreiweis reported that
mice with the human form of FOXP2 learn more quickly
than ordinary mice. She challenged mice to solve a maze
that involved turning either left or right to find a
water reward. A visual clue, such as a star, along with
the texture of the maze's surface, showed the correct
direction to turn.

After eight days of practice, mice with the human form
of FOXP2 learnt to follow the clues to the water 70% of
the time. Normal mice took an additional four days to
reach this level. Schreiweis says that the human form of
the gene allowed mice to more quickly integrate the
visual and tactile clues when learning to solve the
maze.

In humans, she says, the mutation to FOXP2 might have
helped our species learn the complex muscle movements
needed to form basic sounds and then combine these
sounds into words and sentences.

Another MPI team member, Ulrich Bornschein, presented
work at the neuroscience meeting showing that the
changes to brain circuitry that lead to quicker learning
come about with just one of the two amino-acid changes
in the human form of FOXP2. The second mutation may do
nothing.

 "That makes sense," says Genevieve Konopka, a
 neuroscientist at the University of Texas Southwestern
 Medical Center in Dallas, who also studies FOXP2.
 Carnivores, including dogs and wolves, independently
 evolved the other human FOXP2 mutation, with no obvious
 effect on their brains.

Faraneh Vargha-Khadem, a neuroscientist at University
College London who has studied the KE family in which
FOXP2 is mutated, thinks that the new findings could
help explain the gene's role in perfecting the facial
movements involved in speech.

But she does not see how changes in basic learning
circuitry could explain how FOXP2 helps humans to
automatically and effortlessly translate their thoughts
into spoken language. "You are not deciding how you are
going to move your muscles to form these sounds," she
says.

Nature doi:10.1038/nature.2011.9395

References

1 Lai, C. S., Fisher, S. E., Hurst, J. A., Vargha-
Khadem, F. & Monaco, A. P. Nature 413, 519-523 (2001).

2 Enard, W. et al. Nature 418, 869-872 (2002).

3 Krause, J. et al. Curr. Biol. 17, 1908-1912 (2007).

4 Enard, W. et al. Cell 137, 961-971 (2009).

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