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      Retinoic acid induced neural differentiation in a neuroectodermal cell line immortalized by p53 deficiency.

      Journal of Neuroscience Research
      Animals, Antimetabolites, Antineoplastic, pharmacology, Autoradiography, Brain, cytology, Cell Differentiation, drug effects, Cell Line, Chromosomes, physiology, Cytarabine, Growth Substances, Immunohistochemistry, Mice, Nerve Tissue Proteins, metabolism, Neurons, Rats, Stem Cells, Thymidine, Tretinoin, Tumor Suppressor Protein p53, deficiency

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          Abstract

          Neuroepithelial cell lines were established from cerebral vesicles of 9-day-old mouse embryos lacking functional p53 genes (Livingstone et al: Cell 70:923-935, 1992). All-trans retinoic acid (RA) induced bulk formation of neurons both in several p53-deficient neuroepithelial cell lines and in wild-type neural cells derived from early embryonic (E9-E12) forebrain vesicles. Forty-eight-hour treatment with 10(-6) M RA was necessary and sufficient to initiate neuron formation by p53(-/-)-progenitors, but neuronal characteristics appeared with a delay of 3-4 days. The first appearance of cells with astroglial features followed that of neurons with a further delay of 4-5 days. The establishment of neuronal phenotypes involved minimally three rounds of cell cycle. Future neurons were sorted out from substrate-attached cells and were characterized by a specific rearrangement of nestin-immunoreactive filaments. The formation of neuronal phenotypes was not synchronized within the RA-treated cell populations. The data indicate that RA, which promotes the initiation of neural differentiation, cannot function as a direct regulator of cell-fate decisions made by neural progenitor cells.

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