published by Néant I, Mellström B, Gonzales P, Naranjo JR, Moreau M, Leclerc C.
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 is acting.The only known mechanism responsible for a direct action of calcium on gene transcription involves an EF-hand Ca2+ binding protein which belongs to a group of four proteins (Kcnip1 to 4). Kcnip protein can act in a Ca2+-dependent manner as a transcriptional repressor by binding to a specific DNA sequence, the Downstream Regulatory Element (DRE) site. In Xenopus, among the four kcnips, we show that only kcnip1 is timely and spatially present in the presumptive neural territories and is able to bind DRE sites in a Ca2+-dependent manner. The loss of function of kcnip1 results in the proliferation of neural progenitors and in the expansion of the neural plate. Later on this leads to impairment in the development of anterior neural structures. We propose that, in the embryo, at the onset of neurogenesis Kcnip1 is the Ca2+-dependent transcriptional repressor that controls the size of the neural plate.