Corticosteroid receptors in the neural retina and other tissues of the chick embryo

Koehler, Don E.; Moscona, A.A.

doi:10.1016/0003-9861(75)90101-0

Cited by 78 publications

(37 citation statements)

References 30 publications

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“…However, the sum total of the two isoforms was similar in E6 and E10 retina (Fig. 2B), consistent with previous findings that GR protein level (26) and hormone binding activity (23)(24)(25) were similar at these two ages.…”

Section: Differential Expression Of Gr Isorms In E6 and E10supporting

confidence: 81%

“…Supporting this possibility is the finding that overexpression of GR in E6 retina (normally noninducible) resulted in induction of a CAT construct controlled by the promoter of the chicken glutamine synthetase gene (19,22). This developmental increase in GR transcriptional activity is, however, in apparent contrast with findings that the level of hormone binding activity and, presumably, that of GR are similar in E6 and E10 retina (23)(24)(25)(26) (32). The unbound hormone was removed (see Materials and Methods), and the samples were electrophoresed and analyzed.…”

contrasting

confidence: 51%

“…The important point is that the total level of the receptor is similar at both ages, as determined by Western blots (Fig. 2) and hormone binding assays (23)(24)(25)(26). Moreover, the percentage ofGR expressing cells declines as the receptor becomes confined to Muller glia (Fig.…”

Section: Differential Expression Of Gr Isorms In E6 and E10mentioning

confidence: 92%

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Developmental changes in the expression and compartmentalization of the glucocorticoid receptor in embryonic retina.

Gorovits

Ben-Dror

Fox

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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Inducibility by glucocorticoids of the glutamine synthetase gene in chicken embryo retina and the transcriptional activity of the glucocorticoid receptor (GR) greatly increase between embryonic days 6 and 10 (E6, E10), although the level of GR does not markedly change during that time. This apparent discrepancy was investigated by exming the pattern of GR expression in undifferentiated E6 retina and in E10 retina, which consists mostly of differentiated cells. Two GR Isoforms, 90 and 95 kDa, were found to be expressed at both of these ages at a similar total level but in different proportions: in E6 retina the level of the 90-kDa isoform was higher, whereas in E10 retina the 95-kDa receptor was higher.However, following treatment of the retinas with cortisol, the 95-kDa isoform became the predominant receptor at both ages.Immunohistochemical analysis revealed that the cellular localization of GR markedly changed in the course of development: in the undifferentiated E6 retina GR was expressed in virtually all cells, whereas in the more differentiated E10 and E12 retina, GR was detected only in Mfiller glia cells. The latfer represent 20% of the cells in this tissue and are the only cells in which glucocorticoid hormone induces the glutamine synthetase gene.We suggest that the compatmentalization of GR in Muller glia is a majior aspect of the mechanism that modulates receptor activity during retina development and results in the temporal increase in the inducibility of glutamine synthetase and its specific localization in Mfuller glia cells.

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Section: Differential Expression Of Gr Isorms In E6 and E10supporting

confidence: 81%

contrasting

confidence: 51%

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Developmental changes in the expression and compartmentalization of the glucocorticoid receptor in embryonic retina.

Gorovits

Ben-Dror

Fox

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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“…Second, the embryonic hepatic and neural cells that are responsible for production of basal levels of glutamine synthetase might lack the glucocorticoid hormone receptor protein. Although these tissues contain glucocorticoid-binding proteins early in development (21), the binding proteins detected are not necessarily physiological modulators of gene expression. Moreover, because glutamine synthetase expression is likely to be confined to a subset of cells in the brain, measurement of glucocorticoid binding in whole brain homogenates is of limited validity to this issue.…”

Section: Discussionmentioning

confidence: 99%

Tissue-specific regulation of avian glutamine synthetase expression during development and in response to glucocorticoid hormones.

Patejunas¹,

Young²

1987

Mol. Cell. Biol.

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We have isolated a glutamine synthetase cDNA clone derived from chicken retinal RNA. The clone detects a 3.2-kilobase RNA in chicken retina, liver, and brain, based on Northern blotting analysis. The dramatic developmental rise observed for the retinal enzyme, assayed as glutamyl transferase activity, is accompanied by a corresponding rise in this RNA. Injection of hydrocortisone 21-phosphate into the yolk sac of day 10 embryos produces an increase in retinal glutamine synthetase mRNA and glutamyl transferase activity, assayed 4 days after injection. An increase in glutamine synthetase mRNA is also observed within 2 h of incubation of retinal organ cultures with hydrocortisone. Moreover, incubation of these cultures with cycloheximide at a concentration that inhibits protein synthesis by 93% affects neither the basal level nor the hydrocortisonemediated induction of glutamine synthetase mRNA. Although expression of this RNA is developmentally regulated in the brain, steroid hormone injection does not result in a substantial induction. Hepatic glutamine synthetase mRNA is expressed constitutively between embryonic day 10 and 6 days after hatching and is also not hormone inducible. Southern blotting data with chicken DNA digested with EcoRI, HindUI, and BamHI are best interpreted in terms of the cDNA clone detecting only one gene. If so, several cell-type-specific regulatory mechanisms must function to modulate expression of this gene during development.Research primarily by Moscona and colleagues has established that during terminal differentiation of the chick retina levels for the enzyme glutamine synthetase rise dramatically (27). This rise is confined to the Muller glial cells (24) and is temporally correlated with the appearance of circulating corticosteroid hormones (26). Moreover, injection of a glucocorticoid hormone into the yolk sacs of embryos (30) or incubation of retinal organ cultures with a glucocorticoid (28,30) induces production of the enzyme. These observations suggest a physiological role for the glucocorticoid hormone and indicate that the induction of glutamine synthetase in the chicken retina provides a model for the action of glucocorticoid hormones during development.

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“…This developmental pattern of responsiveness to glucocorticoids is retained in the explanted neural retina under organ culture conditions (7). Interestingly, a high level of GR is already present in the retina at early developmental stages (embryonic day 6 [E6], the earliest day analyzed), yet glucocorticoids fail to activate GS expression at this time (6,39). Comparative studies of the kinetics of glucocorticoid binding and of the physicochemical properties of GR from responsive and nonresponsive neural retinas have not revealed any significant differences between them (24).…”

mentioning

confidence: 99%

Involvement of a C/EBP-like protein in the acquisition of responsiveness to glucocorticoid hormones during chick neural retina development.

Ben-Or¹,

Okret²

1993

Mol. Cell. Biol.

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The glucocorticoid receptor in chicken embryonic neural retina is expressed early in ontogeny, yet the tissue's response to the glucocorticoid hormone, i.e., induction of glutamine synthetase (GS), develops later, only during week 2 of ontogeny. Transient transfection of embryonic day 7 (E7) retinal cells, which are nonresponsive to glucocorticoids, with chimeric plasmids containing the chloramphenicol acetyltransferase reporter gene under the control of glucocorticoid-responsive promoters demonstrated that GR in E7 cells is a functional transactivating factor. We show that the limiting transcription factor that controls the developmental acquisition of responsiveness to glucocorticoids is similar to a CCAAT enhancer-binding protein (C/EBP). This protein recognizes a sequence in the promoter of the chick GS gene, which is required for eliciting the glucocorticoid response. Retinal C/EBP-like protein was not detected in the glucocorticoid-nonresponsive (E7) proliferating glioblasts but was found to be present in the glucocorticoid-responsive (E12) postmitotic cells.

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Corticosteroid receptors in the neural retina and other tissues of the chick embryo

Cited by 78 publications

References 30 publications

Developmental changes in the expression and compartmentalization of the glucocorticoid receptor in embryonic retina.

Developmental changes in the expression and compartmentalization of the glucocorticoid receptor in embryonic retina.

Tissue-specific regulation of avian glutamine synthetase expression during development and in response to glucocorticoid hormones.

Involvement of a C/EBP-like protein in the acquisition of responsiveness to glucocorticoid hormones during chick neural retina development.

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