
pmid: 21262462
How the mitosis of neuroepithelial stem cells is restricted to the apical ventricular area remains unclear. In zebrafish, the mosaic eyes(rw306) (moe/epb41l5(rw306)) mutation disrupts the interaction between the putative adaptor protein Moe and the apicobasal polarity regulator Crumbs (Crb), and impairs the maintenance of neuroepithelial apicobasal polarity. While Crb interacts directly with Notch and inhibits its activity, Moe reverses this inhibition. In the moe(rw306) hindbrain, Notch activity is significantly reduced, and the number of cells that proliferate basally away from the apical area is increased. Surprisingly, activation of Notch in the moe(rw306) mutant rescues not only the basally localized proliferation but also the aberrant neuroepithelial apicobasal polarity. We present evidence that the Crb⋅Moe complex and Notch play key roles in a positive feedback loop to maintain the apicobasal polarity and the apical-high basal-low gradient of Notch activity in neuroepithelial cells, both of which are essential for their apically restricted mitosis.
Motor Neurons, Glycogen Synthase Kinase 3 beta, Receptors, Notch, Neuroscience(all), Recombinant Fusion Proteins, Stem Cells, Neuroepithelial Cells, Cell Polarity, Embryonic Development, Mitosis, Nerve Tissue Proteins, Zebrafish Proteins, Animals, Genetically Modified, Glycogen Synthase Kinase 3, Cell Movement, Mutation, Animals, Eye Proteins, Proto-Oncogene Proteins c-akt, Zebrafish
Motor Neurons, Glycogen Synthase Kinase 3 beta, Receptors, Notch, Neuroscience(all), Recombinant Fusion Proteins, Stem Cells, Neuroepithelial Cells, Cell Polarity, Embryonic Development, Mitosis, Nerve Tissue Proteins, Zebrafish Proteins, Animals, Genetically Modified, Glycogen Synthase Kinase 3, Cell Movement, Mutation, Animals, Eye Proteins, Proto-Oncogene Proteins c-akt, Zebrafish
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