Journal
DEVELOPMENTAL DYNAMICS
Volume 235, Issue 9, Pages 2330-2336Publisher
WILEY
DOI: 10.1002/dvdy.20850
Keywords
Notch signaling; Wnt signaling; somite clock; molecular oscillators; paraxial mesoderm; inherited disease; spondylocostal dysostosis
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Funding
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS036437] Funding Source: NIH RePORTER
- NINDS NIH HHS [NS036437] Funding Source: Medline
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A fundamental characteristic of the vertebrate body plan is its segmentation along the anterior-posterior axis. This segmental pattern is established during embryogenesis by the formation of somites, the transient epithelial blocks of cells that derive from the unsegmented presomitic mesoderm. Somite formation involves a molecular oscillator, termed the segmentation clock, in combination with gradients of signaling molecules such as fibroblast growth factor 8, WNT3A, and retinoic acid. Disruption of somitogenesis in humans can result in disorders such as spondylocostal dysostosis, which is characterized by vertebral malformations. This review summarizes recent findings concerning the role of Notch signaling in the segmentation clock, the complex regulatory network that governs somitogenesis, the genes that cause inherited spondylocostal dysostosis, and the mechanisms that regulate bilaterally symmetric somite formation.
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