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Hydrocortisone-mediated regulation of gene expression in embryonic neural retina: induction of glutamine synthetase. |
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| Authors: | A A Moscona |
| Affiliation: | 1. Zhejiang Provincial Key Laboratory for Water Environment and Marine Biological Resources Protection, College of Life and Environmental Science, Wenzhou University, Wenzhou, China;2. Department of Ophthalmology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China;3. The Institute of Translational Medicine, Zhejiang University, Hangzhou, China;1. Department of Biological Structure, University of Washington, Seattle, WA, USA;2. Institute for Stem Cells and Regenerative Medicine, University of Washington, Seattle, WA, USA;1. Department of Bioengineering, University of California, San Diego, United States;2. Department of Ophthalmology, University of California, San Diego, United States;3. Department of Biological Sciences, University of California, San Diego, United States |
| Abstract: | Functional differentiation in the embryonic chick neural retina is marked by a sharp increase in the accumulation of glutamine synthetase (GS). Hydrocortisone and related 11-β-hydroxy corticosteroids induce prematurely GS in the embryonic retina. The induction involves gene expression which results in increased rate of GS synthesis and accumulation. Properties of hydrocortisone receptors in retina cytosol are described and compared with those from other embryonic tissues. Binding of hydrocortisone-receptor complexes to retina nuclei was studied to estimate the number of nuclear binding sites related to GS induction. GS is not inducible in dispersed retina cells; inducibility for this enzyme depends on retinotypic organization of the cells. It is suggested that histotypic cell contacts in the embryonic retina are involved in the mechanisms which control induction by the steroid of this gene-controlled expression characteristic of the differentiation of these cells. |
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