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Blocking Dishevelled signaling in the noncanonical Wnt pathway in sea urchins disrupts endoderm formation and spiculogenesis, but not secondary mesoderm formation
Author(s) -
Byrum Christine A.,
Xu Ronghui,
Bince Joanna M.,
McClay David R.,
Wikramanayake Athula H.
Publication year - 2009
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.21978
Subject(s) - dishevelled , fgf and mesoderm formation , biology , endoderm , mesoderm , microbiology and biotechnology , wnt signaling pathway , blocking (statistics) , signal transduction , embryogenesis , frizzled , embryo , genetics , gastrulation , embryonic stem cell , computer network , computer science , gene
Dishevelled (Dsh) is a phosphoprotein key to beta‐catenin dependent (canonical) and beta‐catenin independent (noncanonical) Wnt signaling. Whereas canonical Wnt signaling has been intensively studied in sea urchin development, little is known about other Wnt pathways. To examine roles of these beta‐catenin independent pathways in embryogenesis, we used Dsh‐DEP, a deletion construct blocking planar cell polarity (PCP) and Wnt/Ca 2+ signaling. Embryos overexpressing Dsh‐DEP failed to gastrulate or undergo skeletogenesis, but produced pigment cells. Although early mesodermal gene expression was largely unperturbed, embryos exhibited reduced expression of genes regulating endoderm specification and differentiation. Overexpressing activated beta‐catenin failed to rescue Dsh‐DEP embryos, indicating that Dsh‐DEP blocks endoderm formation downstream of initial canonical Wnt signaling. Because Dsh‐DEP‐like constructs block PCP signaling in other metazoans, and disrupting RhoA or Fz 5/8 in echinoids blocks subsets of the Dsh‐DEP phenotypes, our data suggest that noncanonical Wnt signaling is crucial for sea urchin endoderm formation and skeletogenesis. Developmental Dynamics 238:1649–1665, 2009. © 2009 Wiley‐Liss, Inc.