Mice With Humanized FOXP2 Have Longer Neurons, Vocalize Differently…

FOXP2 is one of my favorite genes. I studied it extensively while getting my Master’s degree and wrote about it several times on Anthropology.net. For those that do not know much about it, I’ll quickly introduce it. FOXP2 is a transcription factor gene, which means it controls the expression and regulation of many other genes. It is significant in that it is implicated in human language.

I caught news of a new study on FOXP2 today while reading Nicholas Wade’s article in the New York Times about a hot-off-the-press Max Planck study published in Cell on FOXP2. The study comes from Svante Pääbo‘s lab, who created a strain of transgenic mice with the human FOXP2 variant and noted that these mutant mice made whistles that had a slightly lower pitch than ones with the wild-type FOXP2 gene.

The study has been published as an open access paper under the title, “A Humanized Version of Foxp2 Affects Cortico-Basal Ganglia Circuits in Mice.” There are more findings tucked inside the paper that indicate the impact of the human FOXP2. Aside from the changes in dopamine levels, the most interesting one is the increased axonal and dendritic length of medium spiny neurons in the basal ganglia by 80% when compared to FOXP2wt. These neurons coordinate the movement and timing of multiple organ systems. Check out the differences for yourself:

Foxp2(hum) Increases the Length of Dendritic Trees
Foxp2(hum) Increases the Length of Dendritic Trees

The authors hypothesize on the meaning behind this change in these neurons,

“Currently, one can only speculate about the role these effects may have played during human evolution. However, since patients that carry one nonfunctional FOXP2 allele show impairments in the timing and sequencing of orofacial movements (Alcock etal., 2000,Watkins etal., 2002a), one possibility is that the amino acid substitutions in FOXP2 contributed to an increased fine-tuning of motor control necessary for articulation, i.e., the unique human capacity to learn and coordinate the muscle movements in lungs, larynx, tongue and lips that are necessary for speech (Lieberman, 2006). We are confident that concerted studies of mice, humans and other primates will eventually clarify if this is the case.”

What’s also curious is that the mutant FOXP2 mice don’t seem to have any other effects on other organs, despite the fact that FOXP2 is pretty much ubiquitously expressed all over. It seems like the only manifestations of a human variant showed up in the neuron length and dopamine levels of the brain and ultimately vocalization behaviors. This is an excellent paper which investigates the functional differences of FOXP2, and I recommend you downloading a copy and reading it for yourself.

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