How have we acquired our abilities to speak? To vocally communicate a thought? Was the apparatus necessary to make a sound present before adequate intelligence? What can evolution and current comparisons to animal species teach us on the topic? Genetics has brought a new light as to a factor of language, the gene FOXP2. In Ewan Callaway's article ‚??Language gene speeds learning‚?? in Nature, it was stipulated that a mutation in a particular gene may be responsible for the evolution of language via the enhancement of muscle memory for muscles particular to the capacity of speech.
The existence of the gene FOXP2 has been known since the 90's and was reported during the study of a British family where 3 successive generations had a speech impediment associated to a mutation, allowing the expression of only one allelic copy of FOXP2. Also such developmental disorders of language where initially observed in individuals whose SPCH1 locus was translocated from chromosome 7. In this occurrence FOXP2 which encodes for a transcription factor containing a forkhead DNA-binding site was disrupted at the break point, as well as containing a point mutation coding for an invariant amino acid within the proteins' forkhead structure. For these reasons FOXP2 was attributed to play a role in acquiring expressive or receptive language or both.
To understand the particular role it plays in this acquisition, the human FOXP2 sequence was compared to that of other species. The majority of vertebrates have an invariant FOXP2 gene. However, the protein it codes for differs in two amino acids in humans relative to chimpanzees. The nearest common ancestor exhibiting both mutations, found in Homo sapiens but not chimps is the Homo neanderthalensis, suggesting the mutations appeared before the divergence of each species' lineage, 500,000 years ago. This is only circumstantial evidence of the relation between FOXP2 and the development of speech but on the other hand it has clearly been implicated as a major player in the development of brain circuits related to the learning of movement.
In fact, when the human FOXP2 gene was expressed in mice these showed advantages in learning processes comparatively to their counterparts only expressing the unaltered wild type mouse FOXP2. When challenged to find the solution to a maze the humanized rats took 8 days to get a 70% success rate and obtaining the prize while the normal rates took an additional 4 days to obtain these same results. Also, when examining the brains of each it was noticed that the humanized rats had neurons with a greater amount of dendrils and longer extensions and that neurons of the basal ganglia were faster to become unresponsive, phenomena known as long term depression and implicated in the circuits of learning and memory. Apart from these differences it was also observed that human FOXP2 mice were less likely to leave their mothers and had an altered ultrasonic vocalization.
Further investigation revealed that only one of the two differing amino acids of the FOXP2 protein was responsible for these learning enhancements. It is interesting to note that carnivores, such as canines which evolved separately from the human lineage adopted the in-affecting mutation, without obvious consequences on brain function but a clear incapacity for speech relative to humans.
To conclude and by relating these two observations, first that FOXP2 is key to adequate speech and second that it enhances learning we can hypothesize that in humans this gene may have helped in learning the movements of vocal organs necessary to speak and translate thoughts to words. However, one can argue that FOXP2 may be involved in learning the necessary movements for speech but that its effect on the learning circuits might not necessarily be responsible for attributing particular sounds to thought, eventually creating language. Nonetheless, this fact though not proven hasn't been disproved either, cumulatively making FOXP2 a valid candidate responsible for the learning processes that enabled sound to be translated into ideas.