Somitogenesis is the process by which the somites, blocks of mesoderm that give rise to tissues such as the vertebrae, skeletal muscle, cartilage, tendons and skin, are formed. The process occurs under the control of a ‘segmentation clock’: the oscillatory expression of a number of genes and proteins that control cell commitment. The protein paraxial protocadherin (PAPC) is a protocadherin that has been implicated in paraxial mesoderm segmentation; however, the way in which PAPC controls somite formation remains unclear. Now, on p. 664, Olivier Pourquié and colleagues investigate the role of PAPC in chick and mouse somite boundary formation, and demonstrate an entirely novel mechanism for periodic somite formation through the regulated endocytosis of N-cadherin (CDH2). The authors first show that PAPC is cyclically expressed downstream of the segmentation clock, and that PAPC expression colocalizes with CDH2 in the rostral half of the forming somite. In ovo overexpression of the short PAPC isoform in the presomitic mesoderm disrupts apical accumulation of CDH2 and interferes with proper somite morphogenesis. Mechanistically, the authors show how PAPC regulates the endocytosis of CDH2 in the anterior compartment of the forming somite, that is, in regions that have not yet epithelialized. In this way, PAPC regulates the segmental de-adhesion of the somites, which is crucial for their subsequent formation.
Tick tock goes the segmentation clock
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Tick tock goes the segmentation clock. Development 15 February 2017; 144 (4): e0402. doi:
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