Mouse Memory Enhanced By Humanized “Language Gene”

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With mice and men, practice makes perfect, but a mouse with a man’s FOXp2 gene achieves perfection faster.

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We adults envy the ease with which children can learn new languages. How do they remember what all those words mean and even how to pronounce them? How babies learn to speak is equally amazing and is still not fully understood. Genetically engineered mice now offer a clue to these mysteries. Evolutionists also believe they may explain how humans evolved the gift of gab.

“The Language Gene”

The gene FOXP2 is so clearly related to speech and language that it has been dubbed “the language gene.” FOXP2 is a regulatory gene found in humans and many animals—including primates, mice, birds, and fish. About 700 amino acids long, the protein FOXP2 encodes in humans differs by only two amino acids from that of chimps and by only three from mice. Some animals with defective FOXP2 gene are rendered unable to vocalize properly.

Only humans, of course, have the ability to use language, and FOXP2 is necessary for normal human speech. FOXP2 regulates many other genes, so how do we know this? Several members of a Netherlands family with severe difficulty forming words properly as well as problems putting words together and understanding speech were found in 2001 to have a defective FOXP2 gene. Now mice with a humanized FOXP2 gene have revealed a likely role for FOXP2 in learning to produce and understand the spoken word.

Navigating the Maze

Faced with a T-shaped maze in which only one path leads to a treat, mice are taught to associate visual clues and the texture of the floor with the correct path. Then another set of both normal and humanized mice were placed in the maze without the visual clues. Mice with the humanized FOXP2 (mutant mice), although faster in the first experiment, did not learn how to choose the right path any faster than ordinary mice without the visual clues.1 Mutant mice also performed better when they had to transition from what is called place-based (declarative) to response-based (procedural) learning; otherwise they performed about the same as the normal mice. These findings suggest that when there is a scenario where both types of learning are needed, the humanized version of FOXP2 works better.

Linking Symbols to Reality

The researchers say the following:

Our findings prompt the intriguing speculation that the humanization of this gene imparted a facilitated ability to use procedural forms of learning and therefore to shift more rapidly from declarative to procedural forms of learning, a change that could have been important for the emergence of proficient language and speech.2

The T-maze enables researchers to distinguish between ordinary conditioning and decision-making through habitual responses to visual clues. FOXP2 may well help people, infants in particular, learn to habitually use their lips and tongues to shape words properly. After all, once we learn to speak, we do not usually have to concentrate on how to pronounce common words!

Furthermore, children are known to form synaptic connections more efficiently than adults. Since FOXP2 enhances the efficiency of synaptic formation in mice, this study may even offer us a glimpse into the comparative ease with which children acquire second languages.

Neurons, Neurotransmitters, and Learning

Earlier research showed mice with humanized FOXP2 genes grew longer dendrites on some of their nerve cells, made connections between nerve cells better, and had enhanced dopamine levels in a part of the brain associated with making procedural memories into habits. But only with this new research have scientists been able to see what effect these cellular and molecular changes had on actual learning and performance.

Because FOXP2 operates as a regulatory gene in many parts of the brain, coauthor Faraneh Vargha-Khadem cautions against extrapolating to the complexities of actual language acquisition at this point, however, saying, “You can’t extrapolate too much.”1

Evolutionary Extrapolation

Evolutionary scientists show absolutely no hesitancy to extrapolate beyond the observable.

In one area, evolutionary scientists show absolutely no hesitancy to extrapolate beyond the observable—not just to that which remains to be tested but all the way to the cannot-possibly-be-observed realm of human origins. Evolutionists insist that humanity’s ancestors diverged from an ape-like ancestor shared with chimpanzees about 6 million years ago. The FOXP2 protein in humans differs from that in chimps by only two amino acids. Therefore, some evolutionists hail this discovery as the mechanism by which two key mutations presumably paved the way for the human ability to speak.

For instance, senior study author Ann Graybiel explains, “This really is an important brick in the wall saying that the form of the gene that allowed us to speak may have something to do with a special kind of learning, which takes us from having to make conscious associations in order to act to a nearly automatic-pilot way of acting based on the cues around us.”

Neuroscientist Genevieve Konopka of University of Texas Southwestern Medical Center comments that this work “provides new ways to think about the evolution of Foxp2 function in the brain. It suggests that human Foxp2 facilitates learning that has been conducive for the emergence of speech and language in humans. The observed differences in dopamine levels and long-term depression [i.e. the turning off of some neuronal activity] in a region-specific manner are also striking and begin to provide mechanistic details of how the molecular evolution of one gene might lead to alterations in behavior.”

A Master Switch, not an Information-Generator

FOXP2 protein is a genetic switch. It is a transcription factor that binds to DNA to control the production of other proteins. It is not possible that FOXP2 could by switching on any ape-like ancestral genes create the genetic information to evolve into a new, more complex, more nearly human kind of animal. No mechanism in genetics has ever been found to do such a thing. FOXP2 can only turn on or off the information that is already there.

Furthermore, since FOXP2 only controls where and when certain other genes are active, it does not by itself control or enable language ability. FOXP2 makes it possible for other developments to take place. The human form of FOXP2 is a necessary but not sufficient component of linguistic ability.

Liberty University neuroscientist Dr. David Dewitt explains in “FOXP2 and the Non-Evolution of Human Language,” that even referring to FOXP2 as “the language gene” is a grossly misleading oversimplification:

Because FOXP2 is a transcription factor, it cannot control language by itself. Obviously, there are many other proteins involved in the process. Indeed, mutations of FOXP2 primarily result in impairment of orofacial movements preventing those affected from making proper word sounds. Afflicted individuals also show some slight grammar deficiencies. Although the gene is clearly linked to language production, one cannot designate it as the “language gene.” An analogy would be calling the mutation that causes muscular dystrophy (and an inability to walk) a “walking gene.”

Vive La Differénce!

Researchers reporting their results in Proceedings of the National Academy of Sciences write, “Since the time that the human and chimpanzee lineages separated, approximately 6 Mya, two amino acid substitutions have occurred in FOXP2, a higher rate of change than expected given its conservation in mammals.”2

Could two such “substitutions” explain the uniquely human ability to produce and understand speech? Absolutely not! First of all, arbitrarily defining these two differences between human and chimpanzee FOXP2 genes as substitutions or mutations reflects the unverifiable evolutionary assumption that human and chimps share an ancestor! But being different does not demonstrate mutation from a common ancestral source!

Interestingly, chimps, gorillas, and macaques have identical FOXP2 proteins. Evolutionists believe they are separated from mice by 130 million years of evolution. Yet primate FOXP2 differs from mouse FOXP2 by only one amino acid. Despite this greater similarity no one claims mice and chimps are close cousins. The similarity between the FOXP2 in various species points to our common Designer. It does not demonstrate any sort of common ancestry.

Naturally, humans, chimps, and many other animals share a lot of genes. Despite all the hype about similarities in chimp and human DNA, that is exactly what we expect from a wise common Designer, for humans and animals must physically function in the same world. If anything, we should be impressed that God designed this important switch to fulfill many roles so perfectly in us and in so many animals.

We look forward to learning more about the designs by which God our Creator equipped humans alone of all the life He created on the Earth to speak with each other and with Him. Indeed language helps us sort our thoughts and make sense of the world. The uniquely human ability to understand and produce language is just one more reminder that we alone are created in the image of God (Genesis 1:26–27), and we are indeed “fearfully and wonderfully made” (Psalm 139:14).

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Footnotes

  1. Clare Wilson, “Human ‘Language Gene’ Makes Mice Smarter,” New Scientist, September 15, 2014, http://www.newscientist.com/article/dn26216-human-language-gene-makes-mice-smarter.html.
  2. Christiane Schreiweis et al., “Humanized Foxp2 accelerates learning by enhancing transitions from declarative to procedural performance,” Proceedings of the National Academy of Sciences (2014), doi:10.1073/pnas.1414542111.

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