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Please use this identifier to cite or link to this item: http://hdl.handle.net/1783.1/6051
Title: Inhibition of stored Ca2+ release disrupts convergent extension cell movements resulting in abnormal positioning and morphology of the pronephric anlagen in intact zebrafish embryos
Authors: Webb, Sarah E.
Lam, Pui Ying
Leclerc, Catherine
Moreau, Marc
Miller, Andrew L.
Keywords: Ca2+ signaling
Convergence
IP3R
Pronephric anlagen
Zebrafish embryos
Issue Date: May-2009
Citation: Development, Growth & Differentiation, May 2009, v. 51, iss. 4, p. 429-442
Abstract: Ca2+ is a highly versatile intra- and intercellular signal that has been reported to regulate a variety of different pattern-forming processes during early development. To investigate the potential role of Ca2+ signaling in regulating convergence extension (CE) cell movements, and the morphology and positioning of the pronephric anlagen, we treated zebrafish embryos from 11.5 hours post fertilization (hpf; i.e., just before the pronephric anlagen are morphologically distinguishable in the lateral intermediate mesoderm; LM) to 16 hpf, with a variety of membrane permeable pharmacological reagents known to modulate [Ca2+]i. The effect of these treatments on pronephric anlagen morphology and positioning was determined in both fixed and live embryos via in situ hybridization using the pronephic-specific probes, cdh17, pax2.1 and sim1, and confocal imaging of BODIPY ceramide-labelled embryos, respectively. We report that Ca2+ released from intracellular stores via inositol 1,4,5-trisphosphate receptors plays a significant role in the morphology and positioning of the pronephric anlagen, but does not affect the fate determination of the LM cells that form these primordia. Our data suggest that when Ca2+ release is inhibited, the resulting effects on the pronephric anlagen are a consequence of the disruption of normal CE movements of LM cells toward the embryonic midline.
Rights: This is a preprint article published in Development, Growth & Differentiation, © Copyright 2009 Wiley-Blackwell. The original journal article is posted on the Journal's web site at http://www.interscience.wiley.com
URI: http://hdl.handle.net/1783.1/6051
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