Manipulation of Estrogen Synthesis Alters MIR202 Expression in Embryonic Chicken Gonads1
Tissue-specific patterns of microRNA (miRNA) expression contribute to organogenesis during embryonic development. Using the embryonic chicken gonads as a model for vertebrate gonadogenesis, we previously reported that miRNAs are expressed in a sexually dimorphic manner during gonadal sex differentia...
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| Veröffentlicht in: | Biology of reproduction 2011-07, Vol.85 (1), p.22-30 |
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| creator | Bannister, Stephanie C Smith, Craig A Roeszler, Kelly N Doran, Timothy J Sinclair, Andrew H Tizard, Mark L.V |
| description | Tissue-specific patterns of microRNA (miRNA) expression contribute to organogenesis during embryonic development. Using the embryonic chicken gonads as a model for vertebrate gonadogenesis, we previously reported that miRNAs are expressed in a sexually dimorphic manner during gonadal sex differentiation. Being male biased, we hypothesised that up-regulation of microRNA 202* (MIR202*) is characteristic of testicular differentiation. To address this hypothesis, we used estrogen modulation to induce gonadal sex reversal in embryonic chicken gonads and analyzed changes in MIR202* expression. In ovo injection of estradiol-17beta at Embryonic Day 4.5 (E4.5) caused feminization of male gonads at E9.5 and reduced MIR202* expression to female levels. Female gonads treated at E3.5 with an aromatase inhibitor, which blocks estrogen synthesis, were masculinized by E9.5, and MIR202* expression was increased. Reduced MIR202* expression correlated with reduced expression of the testis-associated genes DMRT1 and SOX9, and up-regulation of ovary-associated genes FOXL2 and CYP19A1 (aromatase). Increased MIR202* expression correlated with down-regulation of FOXL2 and aromatase and up-regulation of DMRT1 and SOX9. These results confirm that up-regulation of MIR202* coincides with testicular differentiation in embryonic chicken gonads. |
| doi_str_mv | 10.1095/biolreprod.110.088476 |
| format | Article |
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Using the embryonic chicken gonads as a model for vertebrate gonadogenesis, we previously reported that miRNAs are expressed in a sexually dimorphic manner during gonadal sex differentiation. Being male biased, we hypothesised that up-regulation of microRNA 202* (MIR202*) is characteristic of testicular differentiation. To address this hypothesis, we used estrogen modulation to induce gonadal sex reversal in embryonic chicken gonads and analyzed changes in MIR202* expression. In ovo injection of estradiol-17beta at Embryonic Day 4.5 (E4.5) caused feminization of male gonads at E9.5 and reduced MIR202* expression to female levels. Female gonads treated at E3.5 with an aromatase inhibitor, which blocks estrogen synthesis, were masculinized by E9.5, and MIR202* expression was increased. Reduced MIR202* expression correlated with reduced expression of the testis-associated genes DMRT1 and SOX9, and up-regulation of ovary-associated genes FOXL2 and CYP19A1 (aromatase). Increased MIR202* expression correlated with down-regulation of FOXL2 and aromatase and up-regulation of DMRT1 and SOX9. These results confirm that up-regulation of MIR202* coincides with testicular differentiation in embryonic chicken gonads.</description><identifier>ISSN: 0006-3363</identifier><identifier>EISSN: 1529-7268</identifier><identifier>DOI: 10.1095/biolreprod.110.088476</identifier><language>eng</language><publisher>Society for the Study of Reproduction, Inc</publisher><subject>aromatase inhibitor ; chicken embryo ; E2 ; estradiol-17β ; estradiol/estradiol receptor ; estrogen ; gonad ; microRNA MIR202 ; sex determination ; testis</subject><ispartof>Biology of reproduction, 2011-07, Vol.85 (1), p.22-30</ispartof><rights>2011 by the Society for the Study of Reproduction, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b2556-52915d0e0f099be54edd183f7cbb1cdf52a7e56fb69cf3c65c036d301a5b21363</citedby><cites>FETCH-LOGICAL-b2556-52915d0e0f099be54edd183f7cbb1cdf52a7e56fb69cf3c65c036d301a5b21363</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://bioone.org/doi/pdf/10.1095/biolreprod.110.088476$$EPDF$$P50$$Gbioone$$H</linktopdf><link.rule.ids>314,776,780,26955,27901,27902,52338</link.rule.ids></links><search><creatorcontrib>Bannister, Stephanie C</creatorcontrib><creatorcontrib>Smith, Craig A</creatorcontrib><creatorcontrib>Roeszler, Kelly N</creatorcontrib><creatorcontrib>Doran, Timothy J</creatorcontrib><creatorcontrib>Sinclair, Andrew H</creatorcontrib><creatorcontrib>Tizard, Mark L.V</creatorcontrib><title>Manipulation of Estrogen Synthesis Alters MIR202 Expression in Embryonic Chicken Gonads1</title><title>Biology of reproduction</title><description>Tissue-specific patterns of microRNA (miRNA) expression contribute to organogenesis during embryonic development. Using the embryonic chicken gonads as a model for vertebrate gonadogenesis, we previously reported that miRNAs are expressed in a sexually dimorphic manner during gonadal sex differentiation. Being male biased, we hypothesised that up-regulation of microRNA 202* (MIR202*) is characteristic of testicular differentiation. To address this hypothesis, we used estrogen modulation to induce gonadal sex reversal in embryonic chicken gonads and analyzed changes in MIR202* expression. In ovo injection of estradiol-17beta at Embryonic Day 4.5 (E4.5) caused feminization of male gonads at E9.5 and reduced MIR202* expression to female levels. Female gonads treated at E3.5 with an aromatase inhibitor, which blocks estrogen synthesis, were masculinized by E9.5, and MIR202* expression was increased. Reduced MIR202* expression correlated with reduced expression of the testis-associated genes DMRT1 and SOX9, and up-regulation of ovary-associated genes FOXL2 and CYP19A1 (aromatase). Increased MIR202* expression correlated with down-regulation of FOXL2 and aromatase and up-regulation of DMRT1 and SOX9. These results confirm that up-regulation of MIR202* coincides with testicular differentiation in embryonic chicken gonads.</description><subject>aromatase inhibitor</subject><subject>chicken embryo</subject><subject>E2</subject><subject>estradiol-17β</subject><subject>estradiol/estradiol receptor</subject><subject>estrogen</subject><subject>gonad</subject><subject>microRNA MIR202</subject><subject>sex determination</subject><subject>testis</subject><issn>0006-3363</issn><issn>1529-7268</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqNkNtKAzEQhoMoWKuPIOQFtk6SJrt7WcpaCy2CB_BuydFGt8mSrGDf3i0VvPVqYOb_hpkPoVsCMwI1v1M-dsn2KZoZGXtQVfNSnKEJ4bQuSiqqczQBAFEwJtglusr5A4DMGWUT9LaVwfdfnRx8DDg63OQhxXcb8PMhDDubfcaLbrAp4-36iQLFzXefbM7HuA-42at0iMFrvNx5_TlyqxikyeQaXTjZZXvzW6fo9b55WT4Um8fVernYFIpyLorxRMINWHBQ18ryuTWGVMyVWimijeNUlpYLp0StHdOCa2DCMCCSK0rGf6aIn_bqFHNO1rV98nuZDi2B9qin_dPTjnrak56RYyduHMdg_0n9AEDabWs</recordid><startdate>201107</startdate><enddate>201107</enddate><creator>Bannister, Stephanie C</creator><creator>Smith, Craig A</creator><creator>Roeszler, Kelly N</creator><creator>Doran, Timothy J</creator><creator>Sinclair, Andrew H</creator><creator>Tizard, Mark L.V</creator><general>Society for the Study of Reproduction, Inc</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>201107</creationdate><title>Manipulation of Estrogen Synthesis Alters MIR202 Expression in Embryonic Chicken Gonads1</title><author>Bannister, Stephanie C ; Smith, Craig A ; Roeszler, Kelly N ; Doran, Timothy J ; Sinclair, Andrew H ; Tizard, Mark L.V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b2556-52915d0e0f099be54edd183f7cbb1cdf52a7e56fb69cf3c65c036d301a5b21363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>aromatase inhibitor</topic><topic>chicken embryo</topic><topic>E2</topic><topic>estradiol-17β</topic><topic>estradiol/estradiol receptor</topic><topic>estrogen</topic><topic>gonad</topic><topic>microRNA MIR202</topic><topic>sex determination</topic><topic>testis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bannister, Stephanie C</creatorcontrib><creatorcontrib>Smith, Craig A</creatorcontrib><creatorcontrib>Roeszler, Kelly N</creatorcontrib><creatorcontrib>Doran, Timothy J</creatorcontrib><creatorcontrib>Sinclair, Andrew H</creatorcontrib><creatorcontrib>Tizard, Mark L.V</creatorcontrib><collection>CrossRef</collection><jtitle>Biology of reproduction</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bannister, Stephanie C</au><au>Smith, Craig A</au><au>Roeszler, Kelly N</au><au>Doran, Timothy J</au><au>Sinclair, Andrew H</au><au>Tizard, Mark L.V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Manipulation of Estrogen Synthesis Alters MIR202 Expression in Embryonic Chicken Gonads1</atitle><jtitle>Biology of reproduction</jtitle><date>2011-07</date><risdate>2011</risdate><volume>85</volume><issue>1</issue><spage>22</spage><epage>30</epage><pages>22-30</pages><issn>0006-3363</issn><eissn>1529-7268</eissn><abstract>Tissue-specific patterns of microRNA (miRNA) expression contribute to organogenesis during embryonic development. Using the embryonic chicken gonads as a model for vertebrate gonadogenesis, we previously reported that miRNAs are expressed in a sexually dimorphic manner during gonadal sex differentiation. Being male biased, we hypothesised that up-regulation of microRNA 202* (MIR202*) is characteristic of testicular differentiation. To address this hypothesis, we used estrogen modulation to induce gonadal sex reversal in embryonic chicken gonads and analyzed changes in MIR202* expression. In ovo injection of estradiol-17beta at Embryonic Day 4.5 (E4.5) caused feminization of male gonads at E9.5 and reduced MIR202* expression to female levels. Female gonads treated at E3.5 with an aromatase inhibitor, which blocks estrogen synthesis, were masculinized by E9.5, and MIR202* expression was increased. Reduced MIR202* expression correlated with reduced expression of the testis-associated genes DMRT1 and SOX9, and up-regulation of ovary-associated genes FOXL2 and CYP19A1 (aromatase). Increased MIR202* expression correlated with down-regulation of FOXL2 and aromatase and up-regulation of DMRT1 and SOX9. These results confirm that up-regulation of MIR202* coincides with testicular differentiation in embryonic chicken gonads.</abstract><pub>Society for the Study of Reproduction, Inc</pub><doi>10.1095/biolreprod.110.088476</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Biology of reproduction, 2011-07, Vol.85 (1), p.22-30 |
| issn | 0006-3363 1529-7268 |
| language | eng |
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| source | Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection; BioOne Complete |
| subjects | aromatase inhibitor chicken embryo E2 estradiol-17β estradiol/estradiol receptor estrogen gonad microRNA MIR202 sex determination testis |
| title | Manipulation of Estrogen Synthesis Alters MIR202 Expression in Embryonic Chicken Gonads1 |
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