Abstract
Somitogenesis refers to the segmentation of the paraxial mesoderm, a tissue located on the back of the embryo, into regularly spaced and sized pieces, i.e., the somites. This periodicity is important to assure, for example, the formation of a functional vertebral column. Prevailing models of somitogenesis are based on the existence of a gene regulatory network capable of generating a striped pattern of gene expression, which is subsequently translated into periodic tissue boundaries. An alternative view is that the pre-pattern that guides somitogenesis is not chemical, but of a mechanical origin. A striped pattern of mechanical strain can be formed in physically connected tissues expanding at different rates, as it occurs in the embryo. Here we argue that both molecular and mechanical cues could drive somite periodicity and suggest how they could be integrated.
Highlights
Vertebrates are defined by the presence of the vertebral column
Based on the literature reviewed in the present work, it seems reasonable to think that molecular and mechanical cues would conjointly determine somite periodicity
We suggest that the epithelium of the paraxial mesoderm (PM) is mechanically patterned by differential strain, and that this contributes to the formation of regular somites by fine tuning MESP expression
Summary
Vertebrates are defined by the presence of the vertebral column. This characteristically segmented structure derives primarily from two pieces of mesodermal tissue located at each side of the body axis, the name paraxial mesoderm (PM). In the opposing gradients (OG) model, morphogen gradients in opposite directions would form a bistability window in which cells will suddenly change from immature to a mature state if they switch “on” their clocks This allows the formation of sharp boundaries of gene expression, as those observed in the paraxial mesoderm (C). When the ERK oscillation arrives at the anterior region, it inhibits the activation of the segmentation program in mature cells that express the clock When this oscillation regresses toward the tail, this inhibition is released and cells activate the formation of a somite boundary. In this model the role of FGF signaling is not played by a gradient of positional information, but by the oscillatory behavior of one of its components (E). The absence of somite alterations in zebrafish embryos lacking RA signaling could be explained by the lack of the expanding-NMPs population in fish (Berenguer et al, 2018)
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