Role of a spatial distribution of IP3 receptors in the Ca2+ dynamics of the Xenopus embryo at the mid-blastula transition stage
Article first published online: 21 DEC 2004
Copyright © 2004 Wiley-Liss, Inc.
Volume 232, Issue 2, pages 301–312, February 2005
How to Cite
Díaz, J., Pastor, N. and Martínez-Mekler, G. (2005), Role of a spatial distribution of IP3 receptors in the Ca2+ dynamics of the Xenopus embryo at the mid-blastula transition stage. Dev. Dyn., 232: 301–312. doi: 10.1002/dvdy.20238
- Issue published online: 13 JAN 2005
- Article first published online: 21 DEC 2004
- Manuscript Accepted: 3 SEP 2004
- Manuscript Received: 16 AUG 2004
- Conacyt. Grant Numbers: 128432, G34524-E, 34203-E
- calcium transients;
- calcium waves;
- Xenopus mesodermal induction;
- cell differentiation
Periodic calcium activity correlates temporally with the onset of gene expression in the embryo, suggesting a causal relation between these two events. Calcium transients are elicited by the action of fibroblast growth factor (FGF) through the activation of phospholipase C. In this work, we present a reaction–diffusion model that extends our previous results on the generation of calcium oscillations for a single and two coupled blastomere cells to a meridian of the Xenopus embryo at the mid-blastula transition. In the model, all cells are subject to the same amount of FGF and contain the same concentration of intracellular components, except for the amount of IP3 receptors (IP3R). A bell-shaped distribution of IP3R produces the correct shape of the calcium transients experimentally observed in the Xenopus blastula at stage 8 (mid-blastula transition stage). The model is also capable of predicting period and amplitude values close to the experimental values. In our model, calcium transients induce spatially localized ERK periodic transients that could activate specific nuclear genes, allowing for the regional differentiation of the cells in the zone under the influence of the calcium signal. Developmental Dynamics 232:301–312, 2005. © 2004 Wiley-Liss, Inc.