Embryology - Biology 104, Spring 2006 - Albert Harris and Corey Johnson   TWENTY-SECOND LECTURE - March 10, 2006, by Corey Johnson Neural Crest I Because the neural crest becomes so many cell types and contributes so many cells to the body, it is often called the 4th germ layer. The neural crest cells are derived from the cells at the border of the neural plate and the surface ectoderm. See Figure 8.1 in your book. Both of these tissues contribute to the neural crest. The stages of neural crest migration can be seen as three stages: 1) Epithelial-mesenchymal transition 2) Dispersion 3) Cessation of migration Epithelial-mesenchymal transition. As neural crest cells leave the neural tube they adopt a mesenchymal morphology. Neural tube cells are characterized by the expression of N-CAM (cell adhesion molecule) and N-cadherin. Neural crest cells stop expressing these in conjunction with their loss of adhesion with other cells. The mesenchymal morphology is characterized by an irregular shape with less polarity than an epithelial cell and is migratory. Such cells typically lose preference for other cells and instead, adhere to extracellular matrix molecules. Initiation of migration may depend on transcriptional changes, but in some species it is not. Dispersion/Migration depends upon interactions between the neural crest and the extracellular matrix. Integrins on the surface of NC cells interact with extracellular matrix. Are cell completely dependant upon their environment for guidance, or do they have some sense of where to go (preprogramming) and merely rely on the environment for regional cues? As is often the case, popular thought suggests that NC cell migration depends upon a combination of matrix-directed migration and preprogramming of NC cells. Depending on the A-P origin of the crest, some cells appear to favor one mechanism over another. The control of the migratory path is proposed to follow one or both of the following mechanisms: 1) Contact inhibition: The migrating cells will cease to advance in a particular direction if they encounter another cell. Cells are therefore directed towards areas less densely populated with cells. This is currently believed to be a major mechanism of dispersal. 2) Contact guidance: Physical features within the embryo, such as blood vessels and nerve axons could act as migratory substrata by providing a means of orientation for the migrating cell. How do cells know when to stop migrating? The very fact that cessation of migration occurs implies that cells are programmed to migrate until something stops them. Or do they travel a certain distance and get tired? Cessation is tied up in the process of fate specification and it is difficult to resolve the two. Do cells stop migrating because they are specified to a particular lineage? Or do cells stop migrating because they have arrived at some defined destination? If the later, what tells them they've arrived. What is the nature of that information? When cells find their destination, proliferation takes place. There is evidence that premigratory neural crest is already specified (or at least restricted) to become (or to not become) certain cell types. This is not true of all regions of neural crest in all species. 1) They express some different genes from one another. 2) In culture, single cells will give rise to a certain type(s) of cells, while another NC cell will give rise to different cells. Trunk and Cranial crest do not form the correct structures when transplanted. For example, trunk neural tube will not form cartilage if transplanted to the cranial region (where cartilage is often formed). Despite preprogramming of some NC cells, "Environmental" factors promote differentiation. The end of the migratory route often influences the differentiation of the neural crest. The brain induces the NC to form cranial bones, etc. It's not clear (in my mind) if the differentiation is somehow enhanced, or confirmed by the destination structure, or if they can actually impart identity upon cells. Restriction (a concept we introduced in the first lecture) of NC cells appears to explain the choices that cells make in the course of their fate specification. Some NC cells are incapable of becoming a different cell type: example Regionalization of Neural Crest The neural crest is not the same all over the body. For example, it is clear that some NC will form cartilage in the head, while there is no such derivative in the trunk. Likewise, NC forms sympathetic ganglia in the trunk but not in the head. The question arises, are the differences a result of preprogramming (fate) or do the NC in the trunk fail to form cartilage because they don't receive the proper environmental cues? Cranial Neural Crest: Researchers have found that ablation of migratory neural crest can often result in normal embryos! They thought that neighboring populations either anterior of posterior to the ablated cells might compensate. Instead these cells would not change their fate to become a neighboring segment's neural crest. What happens is that VENTRAL neural tube cells from the segment of ablation regulate to become neural crest to fill in for the lost NC! I think this says something quite important about the degree of segmentation in the embryo and the borders/identities defined by these segments. Migration of cranial NC: movie Trunk Neural Crest: Neural crest posterior to the 6th somite pair is considered trunk NC. Trunk crest will not form cartilage or bone, but will form many structures that the cranial NC does. There are some cells, such as adrenal cells that the cranial crest cannot form. Cardiac neural crest: Cardiac NC is a type of cranial NC that arises from r7. It will travel to the heart where it forms structures associated with the separation of the outflow tract (conus arteriosus) such as the aortic and pulmonary trunk endothelium. It also plays an important role in the separation of these vessels. Parts of the coronary arteries are formed from these cells, too.

 

back to syllabus

back to index page