Language Evolution and Computation Bibliography

Purpose of the review A reduced dosage of the transcription factor FOXP2 leads to speech and language impairments probably owing to deficits in cortical and subcortical neural circuits. Based on evolutionary sequence analysis it has been proposed that the two amino acid substitutions that occurred on the human lineage have been positively selected. Here I review recent studies investigating the functional consequences of these two substitutions and discuss how these first endeavors to study human brain evolution can be interpreted in the context of speech and language evolution. Recent findings Mice carrying the two substitutions in their endogenous Foxp2 gene show specific alterations in dopamine levels, striatal synaptic plasticity and neuronal morphology. Mice carrying only one functional Foxp2, show additional and partly opposite effects suggesting that FOXP2 has contributed to tuning cortico-basal ganglia circuits during human evolution. Evidence from human and songbird studies suggest that this could have been relevant during language acquisition or vocal learning, respectively. Summary FOXP2 could have contributed to the evolution of human speech and language by adapting cortico-basal ganglia circuits. More generally the recent studies allow careful optimism that aspects of human brain evolution can be investigated in model systems such as the mouse.

Language is a uniquely human trait likely to have been a prerequisite for the development of human culture. The ability to develop articulate speech relies on capabilities, such as fine control of the larynx and mouth, that are absent in chimpanzees and other great apes. FOXP2 is the first gene relevant to the human ability to develop language. A point mutation in FOXP2 co-segregates with a disorder in a family in which half of the members have severe articulation difficulties accompanied by linguistic and grammatical impairment. This gene is disrupted by translocation in an unrelated individual who has a similar disorder. Thus, two functional copies of FOXP2 seem to be required for acquisition of normal spoken language. We sequenced the complementary DNAs that encode the FOXP2 protein in the chimpanzee, gorilla, orang-utan, rhesus macaque and mouse, and compared them with the human cDNA. We also investigated intraspecific variation of the human FOXP2 gene. Here we show that human FOXP2 contains changes in amino-acid coding and a pattern of nucleotide polymorphism, which strongly suggest that this gene has been the target of selection during recent human evolution.