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Wnt-5/pipetail functions in vertebrate axis formation as a negative regulator of Wnt/ß-catenin activity
Trudi A. Westfall1,
Ryan Brimeyer1,
Jen Twedt1,
Jean Gladon1,
Andrea Olberding1,
Makoto Furutani-Seiki2, and
Diane C. Slusarski1
1 Department of Biological Sciences, University of Iowa, Iowa City, IA 52242 2 Kondoh Differentiation Signaling Project, Sakyo-ku, 606-8394 Kyoto, Japan
Address correspondence to Diane C. Slusarski, Dept. of Biological Sciences, 312 Biology Building, University of Iowa, Iowa City, IA 52242. Tel.: (319) 335-3229. Fax: (319) 335-1069. email: diane-slusarski{at}uiowa.edu
Abstract:
We provide genetic evidence defining a role for noncanonicalWnt function in vertebrate axis formation. In zebrafish, misexpressionof Wnt-4, -5, and -11 stimulates calcium (Ca2+) release, definingthe Wnt/Ca2+ class. We describe genetic interaction betweentwo Wnt/Ca2+ members, Wnt-5 (pipetail) and Wnt-11 (silberblick),and a reduction of Ca2+ release in Wnt-5/pipetail. Embryos geneticallydepleted of both maternal and zygotic Wnt-5 product exhibitcell movement defects as well as hyperdorsalization and axis-duplicationphenotypes. The dorsalized phenotypes result from increasedß-catenin accumulation and activation of downstreamgenes. The Wnt-5 loss-of-function defect is consistent withCa2+ modulation having an antagonistic interaction with Wnt/ß-cateninsignaling.
Key Words: dorsalventral patterning; calcium; zebrafish; morphogenesis; signal transduction
Abbreviations used in this paper: Ca2+, calcium; CaMKII, Ca2+/calmodulin-dependentkinase; dsh, dishevelled; D-V, dorsal-ventral; hpf, hours postfertilization; IP3R, inositol 1,4,5-triphosphate receptor; mz,maternal-zygotic; ppt, pipetail; slb, silberblick; YSL, yolksyncytial layer; XeC, Xestospongin C.
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