Somitogenesis
Somitogenesis | |
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Details | |
Gives rise to | Somite |
System | Musculoskeletal system |
Identifiers | |
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TH | {{#property:P1694}} |
TE | {{#property:P1693}} |
FMA | {{#property:P1402}} |
Anatomical terminology [[[d:Lua error in Module:Wikidata at line 865: attempt to index field 'wikibase' (a nil value).|edit on Wikidata]]] |
Somitogenesis is the process by which somites form in the developing embryo. Somites are blocks of mesoderm that are located on either side of the neural tube and give rise to important structures such as the vertebrae, ribs, and associated muscles.
Process[edit | edit source]
Somitogenesis begins with the segmentation of the paraxial mesoderm into somites. This process is regulated by a combination of gene expression, signaling pathways, and morphogen gradients. The Notch signaling pathway, Wnt signaling pathway, and FGF signaling pathway play crucial roles in the periodic formation of somites.
Segmentation Clock[edit | edit source]
The segmentation clock is a molecular oscillator that regulates the timing of somite formation. It involves the cyclic expression of genes such as Hes1, Hes7, and Lfng. These genes are expressed in a wave-like pattern in the presomitic mesoderm, leading to the periodic formation of somites.
Determination Front[edit | edit source]
The determination front is a region in the presomitic mesoderm where cells become committed to forming somites. This region is defined by opposing gradients of FGF and retinoic acid. Cells at the determination front are influenced by these gradients to undergo mesenchymal-to-epithelial transition and form somites.
Somite Differentiation[edit | edit source]
Once formed, somites differentiate into several distinct regions:
- The sclerotome, which gives rise to the vertebrae and ribs.
- The dermomyotome, which further differentiates into the dermatome and myotome. The dermatome forms the dermis of the skin, while the myotome forms the skeletal muscles.
Clinical Significance[edit | edit source]
Defects in somitogenesis can lead to congenital abnormalities such as scoliosis, spina bifida, and Klippel-Feil syndrome. Understanding the molecular mechanisms of somitogenesis is crucial for developing therapeutic strategies for these conditions.
See also[edit | edit source]
References[edit | edit source]
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Contributors: Prab R. Tumpati, MD