Activation of Pax6 depends on somitogenesis in the chick embryo cervical spinal cord.

Abstract

Pax6 is a paired-type homeobox gene expressed in discrete regions of the central nervous system. In the spinal cord of 7- to 10-somite-stage chicken embryos, Pax6 is not detected within the caudal neural plate, but is progressively upregulated in the neuroepithelium neighbouring each newly formed somite. In the present study, we accumulate data suggesting that this initial activation of Pax6 is controlled via the paraxial mesoderm in correlation with somitogenesis. First, we observed that high levels of Pax6 expression occur independently of the presence of SHH-expressing cells when neural plates are maintained in culture in the presence of paraxial mesoderm. Second, grafting a somite caudally under a neural plate that has not yet expressed the gene induces a premature activation of Pax6. Furthermore, after the graft of a somite, a period of incubation corresponding to the individualization of a new somite in the host embryo produces an appreciable activation of Pax6. Conversely, Pax6 expression is delayed under conditions where somitogenesis is retarded, i.e., when the rostral part of the presomitic mesoderm is replaced by the same tissue isolated more caudally. Finally, Pax6 transcripts disappear from the neural tube when a somite is replaced by presomitic mesoderm, suggesting that the somite is also involved in the maintenance of Pax6 expression in the developing spinal cord. All together these observations lead to the proposal that Pax6 activation is triggered by the paraxial mesoderm in phase with somitogenesis in the cervical spinal cord.