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Please use this identifier to cite or link to this item: http://hdl.handle.net/1783.1/2263
Title: Calcium transients triggered by planar signals induce the expression of Zic3 gene during neural induction in xenopus
Authors: Leclerc, Catherine
Lee, Michelle
Webb, Sarah E.
Moreau, Marc
Miller, Andrew L.
Keywords: Neural determination
Planar signals
Calcium signalling
Calcium imaging
Aequorin
Zic3
Issue Date: Sep-2003
Citation: Developmental biology, v. 261, iss. 2, September 2003, p. 381-390
Abstract: In intact Xenopus embryos an increase in intracellular Ca2+ in the dorsal ectoderm is both necessary and sufficient to commit the ectoderm to a neural fate. However, the relationship between this Ca2+ increase and the expression of early neural genes is as yet unknown. In intact embryos, studying the interaction between Ca2+ signaling and gene expression during neural induction is complicated by the fact that the dorsal ectoderm receives both planar and vertical signals from the mesoderm. The experimental system may be simplified by using Keller open-face explants where vertical signals are eliminated, thus allowing the interaction between planar signals, Ca2+ transients and neural induction to be explored. We have imaged Ca2+ dynamics during neural induction in open-face explants using aequorin. Planar signals generated by the mesoderm induced localized Ca2+ transients in groups of cells in the ectoderm. These transients resulted from the activation of L-type Ca2+ channels. The accumulated Ca2+ pattern correlated with the expression of the early neural precursor gene, Zic3. When the transients were blocked with pharmacological agents, the level of Zic3 expression was dramatically reduced. These data indicate that in open-face explants, planar signals reproduce Ca2+-signaling patterns similar to those observed in the dorsal ectoderm of intact embryos and that the accumulated effect of the localized Ca2+ transients over time may play a role in controlling the expression pattern of Zic3.
Rights: Developmental biology © copyright (2003) Elsevier. The Journal's web site is located at http://www.sciencedirect.com/
URI: http://hdl.handle.net/1783.1/2263
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