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The Journal of Neuroscience, October 11, 2006, 26(41):10376-10379; doi:10.1523/JNEUROSCI.3379-06.2006

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Symposia and Mini-Symposia
Singing Mice, Songbirds, and More: Models for FOXP2 Function and Dysfunction in Human Speech and Language

Stephanie A. White,¹ Simon E. Fisher,³ Daniel H. Geschwind,² Constance Scharff,⁴ and Timothy E. Holy⁵

Departments of ¹Physiological Science and ²Neurology, University of California, Los Angeles, California 90095, ³Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom, ⁴Max Planck Institute for Molecular Genetics, D-14195 Berlin, Germany, and ⁵Department of Anatomy and Neurobiology, Washington University, St. Louis, Missouri 63110

Correspondence should be addressed to Stephanie A. White, University of California, Los Angeles, Department of Physiological Science, 621 Charles E. Young Drive South, Los Angeles, CA 90095-1606. Email: sawhite{at}ucla.edu

In 2001, a point mutation in the forkhead box P2 (FOXP2) coding sequence was identified as the basis of an inherited speech and language disorder suffered by members of the family known as "KE." This mini-symposium review focuses on recent findings and research-in-progress, primarily from five laboratories. Each aims at capitalizing on the FOXP2 discovery to build a neurobiological bridge between molecule and phenotype. Below, we describe genetic through behavioral techniques used currently to investigate FoxP2 in birds, rodents, and humans for discovery of the neural bases of vocal learning and language.

Key words: basal ganglia; birdsong; brain development; chromatin immunoprecipitation; Forkhead; FOXP2; language; motor learning; song; speech; zebra finch

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Received Aug. 4, 2006; revised Aug. 17, 2006; accepted Aug. 21, 2006.

Correspondence should be addressed to Stephanie A. White, University of California, Los Angeles, Department of Physiological Science, 621 Charles E. Young Drive South, Los Angeles, CA 90095-1606. Email: sawhite{at}ucla.edu

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