@entity71953 a Ca     -dependent @entity71954 regulates the size of the neural plate in XXXX .

@entity71954 @entity71953 @entity1238 @entity9495
In amphibian embryos, our previous work has demonstrated that calcium transients occurring in the dorsal ectoderm at the onset of gastrulation are necessary and sufficient to engage the ectodermal cells into a neural fate by inducing neural specific genes. Some of these genes are direct targets of calcium. Here we search for a direct transcriptional mechanism by which calcium signals are acting. The only known mechanism responsible for a direct action of calcium on gene transcription involves an EF-hand @entity9495      binding protein which belongs to a group of four proteins ( @entity71953 to 4). Kcnip protein can act in a @entity9495     -dependent manner as a @entity71954 by binding to a specific DNA sequence, the Downstream Regulatory Element (DRE) site. In @entity1238 , among the four kcnips, we show that only @entity71953 is timely and spatially present in the presumptive neural territories and is able to bind DRE sites in a @entity9495     -dependent manner. The loss of function of @entity71953 results in the expansion of the neural plate through an increased proliferation of neural progenitors. Later on, this leads to an impairment in the development of anterior neural structures. We propose that, in the embryo, at the onset of neurogenesis @entity71953 is the @entity9495     -dependent @entity71954 that controls the size of the neural plate. This article is part of a Special Issue entitled: 13th European Symposium on Calcium.
