Human FOXP2 Gene Affects Mice
Today's entry was written by the BioLogos Editorial Team. You can read more about what we believe here.
Researchers from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, have genetically engineered mice with the human version of FOXP2, a gene connected to the development of language. The result? The new mice developed more complex nerve cells in the basal ganglia, an area of the brain associated with language. The gene also changed the frequency of the squeaks baby mice utter when separated from their mothers.
The FOXP2 gene first gained prominence after researchers identified a mutation of the gene in three generations of a family from England who all had difficulties speaking, understanding complex sentence structures, and moving muscles to articulate sounds. Since this discovery, researchers have found that the same FOXP2 gene has existed in a more or less stable state in all mammals with the exception of humans, where two significant changes in its coding have occurred. The change, which may have occurred as recently as a hundred thousand years ago, suggests that the evolution of the FOXP2 gene may have contributed to human language development. The mouse study seems to add credence to this hypothesis.
Does the fact that mutation and natural selection may explain the emergence of human language question the need of a God to explain our existence then? Not at all, Dr. Collins says in The Language of God:
"Freeing God from the burden of special acts of creation does not remove Him as the source of the things that make humanity special, and of the universe itself. It merely shows us something of how He operates."
-The Language of God, pages 140-141
To read more about the Max Planck Institute study, see the recent article in The New York Times. The original journal article explaining the study can be found in Volume 137, Issue 5 of Cell. To read more about the FOXP2 gene and other genetic evidence of evolution, be sure to read Dr. Collins' The Language of God.