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First published online September 2, 2003
doi: 10.1242/10.1242/dev.00704
RESEARCH ARTICLE: DEVELOPMENT AND DISEASE |
1 National Institutes of Health, NICHD, LMG, Bldg. 6B, 9000 Rockville Pike,
Bethesda, MD 20892, USA
2 University of Utah, Department of Neurobiology and Anatomy, 401 MREB, Salt
Lake City, UT 84132, USA
3 University of Chicago, Department of Organismal Biology and Anatomy, Chicago,
IL 60637, USA
4 University of California, Irvine, Department of Developmental and Cell
Biology, Irvine, CA 92697, USA
5 Princeton University, Department of Molecular Biology, Princeton, NJ 08544,
USA
6 Max-Planck-Institute for Developmental Biology, Spemannstr.35, 72076,
Tübingen, Germany
7 Howard Hughes Medical Institute, Division of Hematology/Oncology, Children's
Hospital, Boston, MA 02115, USA
Author for correspondence (e-mail:
piotrowski{at}neuro.utah.edu)
Accepted 25 June 2003
The van gogh (vgo) mutant in zebrafish is characterized by defects in the ear, pharyngeal arches and associated structures such as the thymus. We show that vgo is caused by a mutation in tbx1, a member of the large family of T-box genes. tbx1 has been recently suggested to be a major contributor to the cardiovascular defects in DiGeorge deletion syndrome (DGS) in humans, a syndrome in which several neural crest derivatives are affected in the pharyngeal arches. Using cell transplantation studies, we demonstrate that vgo/tbx1 acts cell autonomously in the pharyngeal mesendoderm and influences the development of neural crest-derived cartilages secondarily. Furthermore, we provide evidence for regulatory interactions between vgo/tbx1 and edn1 and hand2, genes that are implicated in the control of pharyngeal arch development and in the etiology of DGS.
Key words: van gogh (vgo), tbx1, endothelin 1, Pharyngeal arch development, DiGeorge syndrome, Endodermal pouches, Aortic arches, Zebrafish
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