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First published online November 21, 2006
doi: 10.1242/10.1242/dev.02694



1 Gene Expression Laboratory, The Salk Institute, La Jolla, CA 92037, USA.
2 Department of Medicine, University of California, San Diego, 9500 Gilman
Drive, La Jolla, CA 92093, USA.
Author for correspondence (e-mail:
pfaff{at}salk.edu)
Accepted 12 October 2006
Members of the T-box transcription factor family (Tbx) are associated with several human syndromes during embryogenesis. Nevertheless, their functions within the developing CNS remain poorly characterized. Tbx20 is expressed by migrating branchiomotor/visceromotor (BM/VM) neurons within the hindbrain during neuronal circuit formation. We examined Tbx20 function in BM/VM cells using conditional Tbx20-null mutant mice to delete the gene in neurons. Hindbrain rhombomere patterning and the initial generation of post-mitotic BM/VM neurons were normal in Tbx20 mutants. However, Tbx20 was required for the tangential (caudal) migration of facial neurons, the lateral migration of trigeminal cells and the trans-median movement of vestibuloacoustic neurons. Facial cell soma migration defects were associated with the coordinate downregulation of multiple components of the planar cell polarity pathway including Fzd7, Wnt11, Prickle1, Vang1 and Vang2. Our study suggests that Tbx20 programs a variety of hindbrain motor neurons for migration, independent of directionality, and in facial neurons is a positive regulator of the non-canonical Wnt signaling pathway.
Key words: Tbx20, Migration, Branchiomotor, Hindbrain, Wnt, Planar cell polarity, Mouse
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