C. Cellular Migration and Re-orientations
Cell migration is a broad term referring to the translation of cells from one location to another. During development, large groups of cells inside the blastocyst migrate to form embryonic layers (endoderm, mesoderm and ectoderm). These cells commit to differentiation programs and evolve into precursors that migrate to their final destinations where they undergo terminal differentiation and produce the different organs and limbs.
A relatively simple example is the migration of muscle precursors from somites to emerging limbs. In the developing brain, neuronal precursors migrate out of the neural tube and take up residence in the distinct layers that will form the brain. These cells move within the layers and send projections (axons and dendrites) through the layers of developing cells to their final targets and then form specific connections. These intercellular connections (synapses) constitute highly specialized interfaces that underlie complex processes such as learning and memory.
Finally, migration of cells from the neural crest is among the best studied embryonic migrations. These cells arise from the top of the neural tube and migrate to a plethora of locations including bone, cartilage, PNS, and skin (melanocytes).
D. Apoptosis
Apoptosis, otherwise called “controlled programmed cell death or cell suicide”, is as much a part of embryonal development as it is for cell proliferation and differentiation. It is controlled by cell genes involved in induction or prevention of programmed cell death (PCD).
During embryogenesis PCD implicates cell elimination, necessary in fashioning of the body/ moulding of tissues. PCD is often used synonymous with the designation apoptosis, which indicates an endogenous cell suicide program by which useless or crippled cells are eliminated.
Electron micrographs of embryos have revealed the presence of numerous cells with the characteristic features of apoptosis. Experiments, in which small tissue fragments were explanted to other regions, have proven that focal apoptosis is under control of genetic, hormonal and local tissue factors. Morphological analysis has shown that most of the ovarian follicles undergo development apoptosis, resulting in follicle atresia. Only a small proportion escapes PCD. Growth factors and estrogens have been identified as follicle survival factors, androgens and gonadotropin releasing hormones are potentiating apoptosis of the follicle.
An exaggerated PCD or a defective apoptosis during embryogenesis may cause developmental abnormalities. Certain viruses can inhibit apoptosis, while metabolic stress or damage of cell structures can induce apoptosis. Therefore not only viral infections, also drugs and chemical or physical injuries during embryogenesis may interfere with the balanced PCD and thus induce malformations. Drugs and therapy designs directed to modulate the apoptotic process will offer new approaches to the prevention of congenital malformations.
Examples: The development of the fingers and toes as well as the atretic changes of the oocytes involves apoptosis.
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