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Activation of Pax6 depends on somitogenesis in the chick embryo cervical spinal cord
F Pituello1, F Medevielle, F Foulquier
1Centre de Biologie du Développement, UMR 5547-CNRS, affiliée à l'INSERM, Université P. Sabatier, 31062 Toulouse cedex, France. pituello@cict.fr
Insights
The paraxial mesoderm regulates Pax6 gene activation during spinal cord development in chicken embryos. Somite formation directly influences Pax6 expression timing and maintenance.
Area of Science:
- Developmental Biology
- Neuroscience
- Gene Regulation
Background:
- Pax6 is a crucial transcription factor for central nervous system development.
- Pax6 expression patterns in the embryonic spinal cord are not fully understood.
- The relationship between somitogenesis and gene expression in the neural tube requires further investigation.
Purpose of the Study:
- To investigate the role of paraxial mesoderm and somitogenesis in regulating Pax6 gene expression.
- To determine if somite formation influences the timing and maintenance of Pax6 expression in the developing spinal cord.
Main Methods:
- In vitro culture of chicken embryonic neural plates with paraxial mesoderm.
- Grafting experiments involving somites and presomitic mesoderm.
- Analysis of Pax6 gene expression patterns using in situ hybridization (implied).
Main Results:
- Pax6 expression in neural plates cultured with paraxial mesoderm is independent of SHH signaling.
- Caudal grafting of somites induces premature Pax6 activation.
- Delayed somitogenesis retards Pax6 expression.
- Replacement of somites with presomitic mesoderm leads to Pax6 transcript disappearance.
Conclusions:
- Pax6 activation in the cervical spinal cord is triggered by the paraxial mesoderm in coordination with somitogenesis.
- Somites play a role in both initiating and maintaining Pax6 expression during spinal cord development.
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.