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Enard, W.* ; Gehre, S.* ; Hammerschmidt, K.* ; Hölter, S.M. ; Blass, T.* ; Somel, M.* ; Brückner, M.K.* ; Schreiweis, C.* ; Winter, C.* ; Sohr, R.* ; Becker, L. ; Wiebe, V.* ; Nickel, B.* ; Giger, T.* ; Müller, U.* ; Groszer, M.* ; Adler, T. ; Aguilar, A.* ; Bolle, I. ; Calzada-Wack, J. ; Dalke, C. ; Ehrhardt, N.* ; Favor, J. ; Fuchs, H. ; Gailus-Durner, V. ; Hans, W. ; Hölzlwimmer, G. ; Javaheri, A. ; Kalaydjiev, S.* ; Kallnik, M. ; Kling, E. ; Kunder, S. ; Moßbrugger, I. ; Naton, B. ; Rácz, I.* ; Rathkolb, B. ; Rozman, J. ; Schrewe, A. ; Busch, D.H.* ; Graw, J. ; Ivandic, B.* ; Klingenspor, M.* ; Klopstock, T.* ; Ollert, M.* ; Quintanilla-Martinez, L. ; Schulz, S. ; Wolf, E.* ; Wurst, W. ; Zimmer, A.* ; Fisher, S.E.* ; Morgenstern, R.* ; Arendt, T.* ; Hrabě de Angelis, M. ; Fischer, J.* ; Schwarz, J.* ; Pääbo, S.*

A humanized version of Foxp2 affects cortico-basal ganglia circuits in mice.

Cell 137, 961-971 (2009)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
It has been proposed that two amino acid substitutions in the transcription factor FOXP2 have been positively selected during human evolution due to effects on aspects of speech and language. Here, we introduce these substitutions into the endogenous Foxp2 gene of mice. Although these mice are generally healthy, they have qualitatively different ultrasonic vocalizations, decreased exploratory behavior and decreased dopamine concentrations in the brain suggesting that the humanized Foxp2 allele affects basal ganglia. In the striatum, a part of the basal ganglia affected in humans with a speech deficit due to a nonfunctional FOXP2 allele, we find that medium spiny neurons have increased dendrite lengths and increased synaptic plasticity. Since mice carrying one nonfunctional Foxp2 allele show opposite effects, this suggests that alterations in cortico-basal ganglia circuits might have been important for the evolution of speech and language in humans. For a video summary of this article, see the Paper-Flick file available with the online Supplemental Data.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords language disorder; inherited speech; transcriptional repressors; ultrasonic vocalization; synaptic plasticity; brain-development; gene; evolution; expression; abnormalities
ISSN (print) / ISBN 0092-8674
e-ISSN 1097-4172
Journal Cell
Quellenangaben Volume: 137, Issue: 5, Pages: 961-971 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place Cambridge, Mass.
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Experimental Genetics (IEG)
Institute of Developmental Genetics (IDG)
Institute of Pathology (PATH)
Institute of Lung Biology (LHI)
Institute of Human Genetics (IHG)