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[FOXP2: from the specific disorder to the molecular biology of language. II. Implications for the ontogenesis and phylogenesis of language].

INTRODUCTION
Cloning FOXP2, the first gene linked to a hereditary variant of specific language impairment (SLI), has allowed researchers to conduct more precise studies into the nature and developmental path of the molecular bases governing the organisation and functioning of the neuron centres responsible for language processing.


DEVELOPMENT
The FOXP2 gene codes for a transcriptional repressor that regulates the proliferation and/or migration of certain neuronal populations in the basal ganglia, cortex, cerebellum and thalamus, and presumably plays a part in the organisation and/or functioning of the fronto-thalamic-striatal system. Moreover, the analysis of the developmental history of the gene suggests that the transcriptional factor FOXP2, although it is quite old, has undergone certain modifications in its secondary structure and has acquired a potential site for phosphorylation for protein kinase C during the recent developmental history of the human species.


CONCLUSIONS
The evidence discussed in this article allows us to suggest FOXP2 plays a significant role in the ontogenetic and phylogenetic development of language. On the one hand, it seems to validate certain general models of linguistic processing that call for a more important role of the subcortical structures (above all for the basal ganglia) in that processing. On the other hand, it seems to suggest that the modifications undergone by FOXP2 would have also allowed certain regions (such as Broca's area) to be recruited for language, either by facilitating the appearance of syntax and/or verbal working memory or by transferring control of articulation to those regions, thereby laying down the foundations for the appearance of spoken language.