Sharing the Roles: An Assessment of Japanese Medaka Estrogen Receptors in Vitellogenin Induction.
Identifieur interne : 001693 ( Ncbi/Checkpoint ); précédent : 001692; suivant : 001694Sharing the Roles: An Assessment of Japanese Medaka Estrogen Receptors in Vitellogenin Induction.
Auteurs : Crystal S D. Lee Pow [États-Unis] ; Erin E. Yost [États-Unis] ; D Derek Aday [États-Unis] ; Seth W. Kullman [États-Unis]Source :
- Environmental science & technology [ 1520-5851 ] ; 2016.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Estradiol, Estrogens, Receptors, Estrogen, Vitellogenins.
- drug effects : Gene Expression, Up-Regulation.
- metabolism : Oryzias.
- Animals, Biological Assay.
Abstract
Teleost fish express at least three estrogen receptor (ER) subtypes. To date, however, the individual role of these ER subtypes in regulating expression of estrogen responsive genes remains ambiguous. Here, we investigate putative roles of three ER subtypes in Japanese medaka (Oryzias latipes), using vitellogenin (VTG) I and II as model genes. We identify specific ligand/receptor/promoter dynamics, using transient transactivation assays that incorporate luciferase reporters comprising 3kb promoter/enhancer regions of medaka VTGI and VTGII genes. Four steroidal estrogens (17β-estradiol, estrone, estriol, and 17α-estradiol) were tested in these assays. Results indicate that all three medaka ERs (mERs) are capable of initiating transactivation of both VTG I and II, with ERβ2 exhibiting greatest activity. Promoter deletion analysis suggests that ligand-specific receptor transactivation and utilization of regional-specific estrogen response elements may be associated with differential activities of each medaka ER. Further, cluster analysis of in vivo gene expression and in vitro transactivation suggests that all three ER subtypes putatively play a role in up-regulation of VTG. Results illustrate that preferential ligand/receptor/promoter interactions may have direct implications for VTG gene expression and other ER-mediated regulatory functions that are relevant to the risk assessment of estrogenic compounds.
DOI: 10.1021/acs.est.6b01968
PubMed: 27391190
Affiliations:
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Kullman</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Sciences, Environmental and Molecular Toxicology Program, North Carolina State University , 850 Main Campus Drive, Raleigh, North Carolina 27606, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biological Sciences, Environmental and Molecular Toxicology Program, North Carolina State University , 850 Main Campus Drive, Raleigh, North Carolina 27606</wicri:regionArea><wicri:noRegion>North Carolina 27606</wicri:noRegion></affiliation></author></analytic><series><title level="j">Environmental science & technology</title><idno type="eISSN">1520-5851</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Biological Assay</term><term>Estradiol (metabolism)</term><term>Estrogens (metabolism)</term><term>Gene Expression (drug effects)</term><term>Oryzias (metabolism)</term><term>Receptors, Estrogen (metabolism)</term><term>Up-Regulation (drug effects)</term><term>Vitellogenins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Dosage biologique</term><term>Expression des gènes ()</term><term>Oestradiol (métabolisme)</term><term>Oestrogènes (métabolisme)</term><term>Oryzias (métabolisme)</term><term>Récepteurs des oestrogènes (métabolisme)</term><term>Régulation positive ()</term><term>Vitellogénines (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Estradiol</term><term>Estrogens</term><term>Receptors, Estrogen</term><term>Vitellogenins</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Oryzias</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Oestradiol</term><term>Oestrogènes</term><term>Oryzias</term><term>Récepteurs des oestrogènes</term><term>Vitellogénines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Biological Assay</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Dosage biologique</term><term>Expression des gènes</term><term>Régulation positive</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Teleost fish express at least three estrogen receptor (ER) subtypes. To date, however, the individual role of these ER subtypes in regulating expression of estrogen responsive genes remains ambiguous. Here, we investigate putative roles of three ER subtypes in Japanese medaka (Oryzias latipes), using vitellogenin (VTG) I and II as model genes. We identify specific ligand/receptor/promoter dynamics, using transient transactivation assays that incorporate luciferase reporters comprising 3kb promoter/enhancer regions of medaka VTGI and VTGII genes. Four steroidal estrogens (17β-estradiol, estrone, estriol, and 17α-estradiol) were tested in these assays. Results indicate that all three medaka ERs (mERs) are capable of initiating transactivation of both VTG I and II, with ERβ2 exhibiting greatest activity. Promoter deletion analysis suggests that ligand-specific receptor transactivation and utilization of regional-specific estrogen response elements may be associated with differential activities of each medaka ER. Further, cluster analysis of in vivo gene expression and in vitro transactivation suggests that all three ER subtypes putatively play a role in up-regulation of VTG. Results illustrate that preferential ligand/receptor/promoter interactions may have direct implications for VTG gene expression and other ER-mediated regulatory functions that are relevant to the risk assessment of estrogenic compounds.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Lee Pow, Crystal S D" sort="Lee Pow, Crystal S D" uniqKey="Lee Pow C" first="Crystal S D" last="Lee Pow">Crystal S D. Lee Pow</name></noRegion><name sortKey="Aday, D Derek" sort="Aday, D Derek" uniqKey="Aday D" first="D Derek" last="Aday">D Derek Aday</name><name sortKey="Kullman, Seth W" sort="Kullman, Seth W" uniqKey="Kullman S" first="Seth W" last="Kullman">Seth W. Kullman</name><name sortKey="Yost, Erin E" sort="Yost, Erin E" uniqKey="Yost E" first="Erin E" last="Yost">Erin E. Yost</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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