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RESEARCH PAPER

iguana encodes a novel zinc-finger protein with coiled-coil domains essential for Hedgehog signal transduction in the zebrafish embryo

¹ Center for Developmental Genetics, School of Medicine and Biomedical Sciences, University of Sheffield, Western Bank, Sheffield S10 2TN, UK; ² Max-Planck-Institut für Entwicklungsbiologie, Abteilung III, Tübingen 72076, Germany; ³ Institute of Molecular and Cell Biology, Singapore 117609, Republic of Singapore

Signaling by lipid-modified secreted glycoproteins of the Hedgehog family play fundamental roles during pattern formation in animal development and in humans; dysfunction of Hedgehog pathway components is frequently associated with a variety of congenital abnormalities and cancer. Transcriptional regulation of Hedgehog target genes is mediated by members of the Gli zinc-finger transcription factors. The relative nuclear concentrations of Gli activator (Gli_act) and repressor (Gli_rep) forms, together with their nucleocytoplasmic trafficking, appear to be critical determinants for target gene expression. Whereas such stringent controls of Gli activity are critical in ensuring appropriate levels of pathway activation, the mechanisms by which these processes are regulated remain inadequately understood. Here, using genetic analysis, we show that the zebrafish iguana gene product acts downstream of the Smoothened protein to modulate Gli activity in the somites of the developing embryo. Positional cloning reveals that iguana encodes the zebrafish ortholog of Dzip1, a novel zinc-finger/coiled-coil domain protein that we show can shuttle between the cytoplasm and nucleus in a manner correlated with Hedgehog pathway activity.

[Keywords: Iguana; Gli; hedgehog signaling; zebrafish; muscle; DzipI]

Received December 23, 2003; revised version accepted April 29, 2004.

Article published online ahead of print. Article and publication date are at http://www.genesdev.org/cgi/doi/10.1101/gad.296004.

⁴ These two authors contributed equally to this work.

⁵ Present address: Department of Anatomy, Downing Street, Cambridge CB2 3DY, United Kingdom.

⁶ Corresponding author. E-MAIL p.w.ingham{at}sheffield.ac.uk; FAX 44-0-114-222-2788.

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