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First published online 4 July 2007
doi: 10.1242/dev.02872

Development 134, 2871-2879 (2007)
Published by The Company of Biologists 2007
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Early developmental specification of the thyroid gland depends on han-expressing surrounding tissue and on FGF signals

Thomas Wendl1,*, Dejan Adzic1,*, Jeffrey J. Schoenebeck2, Steffen Scholpp3,{dagger}, Michael Brand3, Deborah Yelon2 and Klaus B. Rohr1,{ddagger}

1 Institute for Developmental Biology, University of Cologne, Gyrhofstrasse 17, 50923 Köln, Germany.
2 Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016, USA.
3 Max-Planck-Institute of Molecular Cell Biology and Genetics, Pfotenhauerstrasse 108, 01307 Dresden, Germany.

{ddagger} Author for correspondence (e-mail: klaus.rohr{at}uni-koeln.de)

Accepted 24 May 2007

The thyroid is an endocrine gland in all vertebrates that develops from the ventral floor of the anterior pharyngeal endoderm. Unravelling the molecular mechanisms of thyroid development helps to understand congenital hypothyroidism caused by the absence or reduction of this gland in newborn humans. Severely reduced or absent thyroid-specific developmental genes concomitant with the complete loss of the functional gland in the zebrafish hands off (han, hand2) mutant reveals the han gene as playing a novel, crucial role in thyroid development. han-expressing tissues surround the thyroid primordium throughout development. Fate mapping reveals that, even before the onset of thyroid-specific developmental gene expression, thyroid precursor cells are in close contact with han-expressing cardiac lateral plate mesoderm. Grafting experiments show that han is required in surrounding tissue, and not in a cell-autonomous manner, for thyroid development. Loss of han expression in the branchial arches and arch-associated cells after morpholino knock-down of upstream regulator genes does not impair thyroid development, indicating that other han-expressing structures, most probably cardiac mesoderm, are responsible for the thyroid defects in han mutants. The zebrafish ace (fgf8) mutant has similar thyroid defects as han mutants, and chemical suppression of fibroblast growth factor (FGF) signalling confirms that this pathway is required for thyroid development. FGF-soaked beads can restore thyroid development in han mutants, showing that FGFs act downstream of or in parallel to han. These data suggest that loss of FGF-expressing tissue in han mutants is responsible for the thyroid defects.

Key words: Thyroid, Zebrafish, hands off (han, hand2), acerebellar, Fibroblast growth factors, fgf8, Fate mapping, Heart


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