[FOXP2 and the molecular biology of language: new evidence. II. Molecular aspects and implications for the ontogenesis and phylogeny of language].

Abstract:

INTRODUCTION:FOXP2 is the first gene linked to a hereditary variant of specific language impairment and seems to code for a transcriptional repressor that intervenes in the regulation of the development and the functioning of certain thalamic-cortical-striatal circuits. DEVELOPMENT:In the last three years, significant progress has been made in the determination of the structural and functional properties of the gene. These advances essentially have to do with the precise analysis of the most important structural motifs of the protein that it codes for and the main parameters that determine its interaction with DNA. They also concern the determination of the functional and behavioural properties in vivo of the main isoforms of the FOXP2 protein, the exact determination of the pattern of expression of new orthologues of the gene, and the identification of the different target genes for factor FOXP2. CONCLUSIONS:This new evidence suggests that protein FOXP2 protein has a high degree of versatility in vivo when it comes to binding to DNA; that its different isoforms are biologically functional; and that the FOXP2 gene is functional during embryonic development and during the adult phase. It also suggests that it is involved in the development and/or functioning of the thalamic-cortical-striatal circuits associated to motor planning, sequential behaviour and procedural learning (a significant saving in developmental terms of the regulatory mechanism in which the gene is involved), as well as the accuracy of the models of linguistic processing that consider language to be, to a large extent, the result of an interaction between certain cortical and subcortical structures.

journal_name

Rev Neurol

journal_title

Revista de neurologia

authors

Benítez-Burraco A

subject

Has Abstract

pub_date

2008-03-16 00:00:00

pages

351-9

issue

6

eissn

0210-0010

issn

1576-6578

pii

rn2008124

journal_volume

46

pub_type

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