Calcium Signaling and Cell Fate Determination During Neural Induction in Amphibian Embryos

Abstract

Experiments performed with isolated ectoderm explants from Xenopus laevis embryos suggest that neural determination is a “by default” mechanism, which occurs when bone morphogenetic proteins (BMPs) are antagonized by extracellular antagonists. BMPs are responsible for the determination of epidermis. However, Ca²⁺ imaging of intact Xenopus embryos reveals patterns of Ca²⁺ transients that are generated via the activation of dihydropyridine (DHP)-sensitive Ca²⁺ channels in the dorsal ectoderm but not in the ventral ectoderm. These increases in the concentration of intracellular Ca²⁺ ([Ca²⁺]_i) appear to be necessary and sufficient to direct the ectodermal cells toward a neural fate as increasing the [Ca²⁺]_i artificially results in neuralization of the ectoderm. The construction of a subtractive cDNA library between untreated and caffeine-treated (i.e., to increase [Ca²⁺]_i) ectoderms led to the identification of early Ca²⁺-sensitive target genes expressed in the neural territories. One of these genes, which encodes an arginine methyl transferase, was found to control the expression of the early proneural gene, Zic3. Here, we discuss the possibility of an alternative model to the current “by default” mechanism, where Ca²⁺ plays a central regulatory role, and epidermal determination only occurs when the Ca²⁺-dependent signaling pathways are inactive.