Involvement of SIP1 in positioning of somite boundaries in the mouse embryo.
Periodical production of somites provides an excellent model system for understanding genesis of metameric structures underlying embryonic development. This study reports production of somites with roughly half rostro-caudal length in homozygous Sip1 (Smad-interacting protein 1) knockout mouse embryos. This altered periodicity of somitogenesis is caused by the rostral expansion of the expression domain of genes involved in the maintenance of unsegmented state of paraxial mesoderm, e.g., Fgf8, Wnt3a, Dll3, and Tbx6. This is accompanied by the rostral extension of oscillatory gene expression such as L-fng, Hes7, and Dll1, and the rostrally shifted termination of Raldh2 expression that continues from the anterior embryonic side. The phenotype of Sip1-/- embryo introduces a new molecular component SIP1 in positioning of somite boundaries, and provides support for the current "clock and wavefront" model.[1]References
- Involvement of SIP1 in positioning of somite boundaries in the mouse embryo. Maruhashi, M., Van De Putte, T., Huylebroeck, D., Kondoh, H., Higashi, Y. Dev. Dyn. (2005) [Pubmed]
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