A protein in the brain that has been linked to the development of human language may push developing neurons to reach out and touch someone—or, at least, other brain cells, according to a new study. Such early links could organize the cell-to-cell connections critical for learning complex tasks later in life, including reciting Dr. Seuss, researchers say.
Researchers first identified the FOXP2 gene and its protein in 2001. The study involved a family that had difficulty pronouncing and understanding words, and since then scientists have suspected that the gene may have played a role in the evolution of human language. It even appears to be important to "speech" in other animals: zebra finches with low levels of the FOXP2 protein, for example, can't learn the songs that other birds sing.
Most studies of FOXP2 have focused on its effects post-birth, says Simon Fisher, a neurogeneticist at the Max Planck Institute for Psycholinguistics in Nijmegen, Netherlands. So scientists have been unclear about its role in very early brain building.
To tease this out, Fisher and colleagues turned to embryonic mice. The team screened thousands of known genes in whole mice brains, looking for those switched on or off by the FOXP2 protein. In brain tissue bathed in high concentrations of FOXP2, the protein kicked about 160 genes into gear. Another 180 genes in these cells slowed down protein production. All of this suggests that FOXP2 is a "hub in a network of genes which might be important," Fisher says.
FOXP2 casts a wide net and also disproportionately oversees genes involved in brain cell organization and growth, most notably the growth of neuronal neurites, appendages that reach out to other neurons. In fact, many neurons in the brains of mice lacking functional FOXP2 proteins had noticeably stubbier appendages, Fisher's team reports online today in PLoS Genetics.
Such appendage stretching could be critical for learning. Early brain cells tend to chat with too many other neurons initially, explains Peter Carlsson, a developmental biologist at the University of Gothenburg in Sweden, who was not involved with the study. But when animals learn, those excess limbs get lopped off until only a few critical connections remain. Without FOXP2, it's possible that "you have less starting material for that pruning or adaptation," he says.
Still, the study doesn't fully explain how FOXP2 regulates human speech, says Sridhar Hannenhalli, a computational biologist at the University of Maryland, College Park. "Neurite growth in any arbitrary neuron, it's not going to lead to language development."
The answer may lie more in motor than language skills, Fisher says. Mice lacking the FOXP2 protein have trouble completing basic movement tasks, such as running on a rodent wheel. And as anyone who's read Dr. Seuss's There's a Wocket in My Pocket! aloud knows, speaking is a taxing feat, involving complex lip pursing and tongue undulations: "It's one of the most challenging things we do."