Target type: biologicalprocess
The movement of trunk neural crest cells from the neural tube, travelling ventrally through the anterior half of each sclerotome. Trunk neural crest cells that remain in the sclerotome form the dorsal root ganglia containing the sensory neurons. Trunk neural crest cells that continue more ventrally form the sympathetic ganglia, the adrenal medulla, and the nerve clusters surrounding the aorta. [GOC:bf, GOC:mat, GOC:PARL, PMID:16319111, PMID:19386662]
Ventral trunk neural crest cells (NCCs) embark on a remarkable journey during embryonic development, migrating from the neural tube to their final destinations. This journey is essential for the formation of a diverse array of tissues, including peripheral nerves, pigment cells, and endocrine cells. Here's a detailed description of the process:
**1. Origin and Specification:** NCCs arise from the dorsal region of the neural tube, specifically at the border between the neural plate and the non-neural ectoderm. These cells acquire a migratory fate through a complex interplay of signaling molecules, including Wnt, BMP, and FGF.
**2. Epithelial-to-Mesenchymal Transition (EMT):** Prior to migration, NCCs undergo a critical transformation from an epithelial state to a mesenchymal state. This involves changes in cell adhesion, cytoskeletal organization, and gene expression. The loss of cell-cell contacts allows NCCs to detach from the neural tube and initiate their journey.
**3. Migratory Pathways:** NCCs migrate along well-defined pathways that are influenced by both intrinsic cues within the cells and extrinsic cues from the surrounding environment. These pathways are typically characterized by the presence of extracellular matrix molecules, such as laminin and fibronectin, which provide adhesion sites and guidance signals.
**4. Chemoattraction and Chemorepulsion:** NCCs navigate their migratory routes through the interplay of chemoattractants and chemorepellents. These molecules, secreted from target tissues or surrounding cells, act as chemical gradients that guide NCCs towards their final destinations. For example, netrin-1, a chemoattractant, guides NCCs towards the ventral midline, while Slit2, a chemorepellent, prevents them from crossing the midline.
**5. Cell-Cell Interactions:** During migration, NCCs interact with each other and with other cell types, such as mesenchymal cells and glial cells. These interactions play a crucial role in regulating migration speed, direction, and the formation of migratory streams.
**6. Differentiation:** Once NCCs reach their target locations, they undergo differentiation into various cell types. This process is influenced by both the intrinsic properties of the NCCs and the extrinsic signals from the surrounding environment. For example, NCCs that migrate to the periphery of the embryo differentiate into melanocytes (pigment cells), while those that migrate to the ventral midline differentiate into sympathetic neurons.
**7. Regulation of Migration:** The precise timing, direction, and differentiation of NCCs are tightly regulated by a complex interplay of genetic and environmental factors. Mutations in genes involved in NCC migration can lead to developmental defects, such as neurocristopathies, which affect the development of various tissues and organs.'
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Protein | Definition | Taxonomy |
---|---|---|
Neuropilin-1 | A neuropilin-1 that is encoded in the genome of human. [PRO:WCB, UniProtKB:O14786] | Homo sapiens (human) |
Compound | Definition | Classes | Roles |
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ala-thr-trp-leu-pro-pro-arg | |||
EG00229 | benzothiadiazole; dicarboxylic acid monoamide; L-arginine derivative; secondary carboxamide; sulfonamide; thiophenes | angiogenesis inhibitor; antineoplastic agent; neuropilin receptor antagonist |