期刊
HUMAN MOLECULAR GENETICS
卷 28, 期 5, 页码 701-717出版社
OXFORD UNIV PRESS
DOI: 10.1093/hmg/ddy372
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资金
- Ecole des Neurosciences de Paris-ENP
- Inserm/CNRS ATIP-AVENIR programme
- Institute de France/Fondation NRJ
- Fondation pour la Recherche Medicale en France-FRM [DEA20090615981]
- Agence nationale de la recherche [ANR-13-ISV4-0004]
- 'Investissements d'Avenir' program [ANR-11-IDEX-0004-02]
- NIH [1R01MH107515, 5R01HG008687]
- Agence Nationale de la Recherche (ANR) [ANR-13-ISV4-0004] Funding Source: Agence Nationale de la Recherche (ANR)
Genetic disruptions of the forkhead box transcription factor FOXP2 in humans cause an autosomal-dominant speech and language disorder. While FOXP2 expression pattern are highly conserved, its role in specific brain areas for mammalian social behaviors remains largely unknown. Here we studied mice carrying a homozygous cortical Foxp2 deletion. The postnatal development and gross morphological architecture of mutant mice was indistinguishable from wildtype (WT) littermates. Unbiased behavioral profiling of adult mice revealed abnormalities in approach behavior towards conspecifics as well as in the reciprocal responses of WT interaction partners. Furthermore mutant mice showed alterations in acoustical parameters of ultrasonic vocalizations, which also differed in function of the social context. Cell type-specific gene expression profiling of cortical pyramidal neurons revealed aberrant regulation of genes involved in social behavior. In particular Foxp2 mutants showed the downregulation of Mint2 (Apba2), a gene involved in approach behavior in mice and autism spectrum disorder in humans. Taken together these data demonstrate that cortical Foxp2 is required for normal social behaviors in mice.
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