We have characterised the patterning capacity of the notochord on the somite using the murine Pax-1 gene as a ventral, and Pax-3 as a dorsal molecular marker. As model systems we chose the four mouse notochord mutants Brachyury curtailed (Tc), Danforth's short tail (Sd), Pintail (Pt) and truncate (tc). Their notochord either is initially absent or progressively degenerates. The use of these mutants enabled us to compare the effect of graded notochord deficiencies. All four mutants show premature termination of the vertebral column. This phenotype can be traced back to an impaired dorsoventral specification of the somites. In tc/tc and Tc/+ embryos the notochord in the affected regions is missing from the beginning. Consequently, Pax-1 is never activated, and Pax-3 remains to be expressed in the entire somite. In contrast, in Sd and Pt embryos the notochord secondarily degenerates. At the end of the prevertebral column Pax-1 expression is lost, while the Pax-3 signal occupies the former Pax-1 expressing zone. The altered pax gene expression in the notochord mutants suggests that the notochord is required for two processes in the dorsoventral patterning of the somite: first the induction of ventral structures, and second the maintenance of the ventral fate.
|Number of pages||19|
|Journal||Mechanisms of Development|
|Publication status||Published - Dec 1993|
- Cell Differentiation
- Gene Expression
- Genetic Markers
- Mice, Inbred Strains