Format

Send to

Choose Destination
Hum Mol Genet. 2018 Oct 23. doi: 10.1093/hmg/ddy372. [Epub ahead of print]

Altered social behavior in mice carrying a cortical Foxp2 deletion.

Author information

1
Inserm, Institut du Fer à Moulin, Sorbonne Université, UMR-S839, Paris, France.
2
Department of Genetics, Washington University School of Medicine, St. Louis, Missouri, USA; Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri, USA.
3
Anthropology & Human Genomics, Department of Biology II, Ludwig-Maximilians-University, Planegg-Martinsried, Germany.
4
Institut des Neurosciences Paris-Saclay, Centre National de la Recherche Scientifique UMR 9197, Orsay, France.

Abstract

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 (USV), 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.

PMID:
30357341
DOI:
10.1093/hmg/ddy372

Supplemental Content

Full text links

Icon for Silverchair Information Systems
Loading ...
Support Center