Journal
JOURNAL OF CELL BIOLOGY
Volume 162, Issue 5, Pages 889-898Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200303107
Keywords
dorsal-ventral patterning; calcium; zebrafish; morphogenesis; signal transduction
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We provide genetic evidence defining a role for noncanonical Writ function in vertebrate axis formation. In zebrafish, misexpression of Wnt-4, -5, and -11 stimulates calcium (Ca2+) release, defining the Wnt/Ca2+ class. We describe genetic interaction between two Wnt/Ca2+ members, Wnt-5 (pipetail) and Wnt-11 (silberblick), and a reduction of Ca2+ release in Wnt-5/pipetail. Embryos genetically depleted of both maternal and zygotic Wnt-5 product exhibit cell movement defects as well as hyperdorsalization and axis-duplication phenotypes. The dorsalized phenotypes result from increased beta-catenin accumulation and activation of downstream genes. The Wnt-5 loss-of-function defect is consistent with Ca2+ modulation having an antagonistic interaction with Wnt/beta-catenin signaling.
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