paraxial mesodermal cell fate commitment

Definition

Target type: biologicalprocess

The process in which a cell becomes committed to become a paraxial mesoderm cell. [GOC:dgh]

Paraxial mesoderm, the precursor tissue to the axial skeleton and skeletal muscles, undergoes a complex process of cell fate commitment driven by a cascade of molecular signaling pathways. This process, which begins during gastrulation, involves a tightly regulated interplay between transcription factors, signaling molecules, and epigenetic modifications.

During gastrulation, the paraxial mesoderm forms from the primitive streak, a transient structure at the posterior end of the embryo. As cells migrate away from the primitive streak, they express the transcription factor Brachyury (T) and become specified as mesoderm. Within the mesoderm, a specific set of genes, including the Wnt and FGF signaling pathways, are activated, defining the paraxial mesodermal fate. These genes, in turn, regulate the expression of other key transcription factors, such as Pax3 and Pax7, which play crucial roles in the subsequent development of the somites.

The paraxial mesoderm is then segmented into repeating units called somites. Somite formation, known as somitogenesis, is a complex process that involves the periodic expression of genes that regulate the formation of somite boundaries. This periodic gene expression is controlled by a molecular clock, which involves a feedback loop of oscillating gene expression. As somites form, cells within each somite undergo further differentiation to generate specific cell types, including myoblasts (muscle precursor cells), chondrocytes (cartilage precursor cells), and sclerotome (bone precursor cells).

The commitment of paraxial mesodermal cells to a specific fate is influenced by a combination of signaling pathways, including Wnt, FGF, and Shh. These pathways interact with each other and with transcription factors to regulate the expression of specific genes that define each cell type. For example, Wnt signaling promotes myoblast formation, while Shh signaling promotes sclerotome formation.

Epigenetic modifications, such as DNA methylation and histone acetylation, also play important roles in paraxial mesoderm cell fate commitment. These modifications can alter gene expression patterns, contributing to the establishment and maintenance of specific cell fates.

In summary, paraxial mesodermal cell fate commitment is a tightly regulated process that involves a complex interplay between signaling pathways, transcription factors, and epigenetic modifications. This process ensures the proper formation of the axial skeleton and skeletal muscles, critical components of the vertebrate body.'
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