The cranial motor neuron development is very vulnerable

This model is well suited to detect changes in cranial motor nerves III, V, VII and X. Nestin MO injection is accompanied by disappearance of III and IV, reduction of V and VII and aberrant positioning of X. These results indicate that the cranial motor neuron development is very vulnerable to nestin defects. Cranial axons are reduced or even abolished in nestin MO-treated embryos, most prominently in the tectum. Both eyes are small and the retina and lens are underdeveloped in nestin knockdown fish. These developmental defects are correlated with increased retinal apoptosis. It has been shown that Nestin is expressed in murine retinal progenitor cells. It is also reported in zebrafish that Nestin is expressed in the retinal ganglion cell layer and ciliary marginal zone, which constitutes the retinal proliferation zone. Our whole mount in situ hybridization results are consistent with expression of nestin in embryonic eyes, presumably in the retinal progenitor cells. It is reasonable to assume that, like its role in neuronal development, Nestin is essential for the retinal development primarily by controlling the retinal progenitor cell survival. Lens development may require Nestin for similar reasons. Nestin was reported to be expressed in the epithelium of lens vesicle. Nestin MO may induce apoptosis of the epithelial progenitor cells, resulting in defective lens development and organization. In summary, nestin is widely expressed in developing zebrafish brain and eyes, especially in the neural, retinal and lens epithelial progenitor cells. It plays a crucial role in protecting progenitor cells from apoptosis U73122 thereby facilitating progenitor cell development into neurons, glial cells, motor nerves, retina and lens. Its deficiency leads to enhanced progenitor cell apoptosis and defective brain, eye and cranial nerve development. Mitochondria are essential organelles, derived in the first BAR501 eukaryotes from intracellular bacterial symbionts. Phylogenetic reconstructions show that these endosymbionts were of aproteobacterial descent, and key aspects of mitochondrial biology evolved from the bacterial ancestor.