Isolation and characterization of three estrogen receptor transcripts in Oreochromis mossambicus (Peters)
Exposure of aquatic organisms to 17β-estradiol (E 2) induces a variety of estrogen-responsive genes, including vitellogenin ( vtg)—the precursor protein of egg yolk in oviparous animals and to date the single most used gene product in screening for estrogenic endocrine disruption. Transcription regu...
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Veröffentlicht in: | The Journal of steroid biochemistry and molecular biology 2010-03, Vol.119 (1), p.26-34 |
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Sprache: | eng |
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Zusammenfassung: | Exposure of aquatic organisms to 17β-estradiol (E
2) induces a variety of estrogen-responsive genes, including vitellogenin (
vtg)—the precursor protein of egg yolk in oviparous animals and to date the single most used gene product in screening for estrogenic endocrine disruption. Transcription regulation of
vtg by E
2 is dependent on binding of the ligand (E
2) to a specific nuclear receptor (estrogen receptor,
ESR) which in turn binds to an estrogen responsive element (ERE) in the promoter of
vtg. Since a local tilapiine,
Oreochromis mossambicus (Peters), is targeted as a model for estrogenic endocrine disruption in Southern Africa, a platform of knowledge is necessary for the ontogenic and tissue specific behavior of
ESR in this species before
vtg levels can be interpreted in relation to such endocrine disruption. Therefore, three
ESR cDNA sequences (
ESR1,
ESR2a and
ESR2b) in
O. mossambicus were isolated and QPCR protocols were developed to ascertain their quantitative transcript levels in adult brain, gonadal and hepatic tissues.
ESR1 transcript levels were highest in female liver tissue compared to males and other tissues, whereas the levels for
ESR2a and
b were not statistically significantly different between male and female tissues. Quantitative gene levels during development demonstrated a sharp increase in
ESR1 during the stage of gonad differentiation (50–60 days post-fertilization) in this species. Finally, an induction experiment in adult male liver tissue confirms the upregulation of
ESR1 by E
2. |
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ISSN: | 0960-0760 1879-1220 |
DOI: | 10.1016/j.jsbmb.2009.12.002 |