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DMRT1 prevents female reprogramming in the postnatal mammalian testis
Sex in mammals is determined in the fetal gonad by the presence or absence of the Y chromosome gene Sry, which controls whether bipotential precursor cells differentiate into testicular Sertoli cells or ovarian granulosa cells. This pivotal decision in a single gonadal cell type ultimately controls...
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| Published in: | Nature (London) 2011-08, Vol.476 (7358), p.101-104 |
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| creator | Matson, Clinton K Murphy, Mark W Sarver, Aaron L Griswold, Michael D Bardwell, Vivian J Zarkower, David |
| description | Sex in mammals is determined in the fetal gonad by the presence or absence of the Y chromosome gene Sry, which controls whether bipotential precursor cells differentiate into testicular Sertoli cells or ovarian granulosa cells. This pivotal decision in a single gonadal cell type ultimately controls sexual differentiation throughout the body. Sex determination can be viewed as a battle for primacy in the fetal gonad between a male regulatory gene network in which Sry activates Sox9 and a female network involving WNT/β-catenin signalling. In females the primary sex-determining decision is not final: loss of the FOXL2 transcription factor in adult granulosa cells can reprogram granulosa cells into Sertoli cells. Here we show that sexual fate is also surprisingly labile in the testis: loss of the DMRT1 transcription factor in mouse Sertoli cells, even in adults, activates Foxl2 and reprograms Sertoli cells into granulosa cells. In this environment, theca cells form, oestrogen is produced and germ cells appear feminized. Thus Dmrt1 is essential to maintain mammalian testis determination, and competing regulatory networks maintain gonadal sex long after the fetal choice between male and female. Dmrt1 and Foxl2 are conserved throughout vertebrates and Dmrt1-related sexual regulators are conserved throughout metazoans. Antagonism between Dmrt1 and Foxl2 for control of gonadal sex may therefore extend beyond mammals. Reprogramming due to loss of Dmrt1 also may help explain the aetiology of human syndromes linked to DMRT1, including disorders of sexual differentiation and testicular cancer. |
| doi_str_mv | 10.1038/nature10239 |
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This pivotal decision in a single gonadal cell type ultimately controls sexual differentiation throughout the body. Sex determination can be viewed as a battle for primacy in the fetal gonad between a male regulatory gene network in which Sry activates Sox9 and a female network involving WNT/β-catenin signalling. In females the primary sex-determining decision is not final: loss of the FOXL2 transcription factor in adult granulosa cells can reprogram granulosa cells into Sertoli cells. Here we show that sexual fate is also surprisingly labile in the testis: loss of the DMRT1 transcription factor in mouse Sertoli cells, even in adults, activates Foxl2 and reprograms Sertoli cells into granulosa cells. In this environment, theca cells form, oestrogen is produced and germ cells appear feminized. Thus Dmrt1 is essential to maintain mammalian testis determination, and competing regulatory networks maintain gonadal sex long after the fetal choice between male and female. Dmrt1 and Foxl2 are conserved throughout vertebrates and Dmrt1-related sexual regulators are conserved throughout metazoans. Antagonism between Dmrt1 and Foxl2 for control of gonadal sex may therefore extend beyond mammals. Reprogramming due to loss of Dmrt1 also may help explain the aetiology of human syndromes linked to DMRT1, including disorders of sexual differentiation and testicular cancer.</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>DOI: 10.1038/nature10239</identifier><identifier>PMID: 21775990</identifier><identifier>CODEN: NATUAS</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Aging - physiology ; Animals ; Animals, Newborn ; Cell Transdifferentiation ; Female ; Females ; Feminization - genetics ; Forkhead Box Protein L2 ; Forkhead Transcription Factors - biosynthesis ; Forkhead Transcription Factors - metabolism ; Gene Expression Regulation ; Genes ; Genetics ; Granulosa Cells - cytology ; Granulosa Cells - metabolism ; Male ; Mice ; Models, Biological ; Ovary - cytology ; Ovary - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Rodents ; Sertoli Cells - cytology ; Sertoli Cells - metabolism ; Sex Characteristics ; Sex Determination Processes - genetics ; Sex Determination Processes - physiology ; Sex Differentiation - genetics ; Sex Differentiation - physiology ; SOX9 Transcription Factor - metabolism ; Testis - cytology ; Testis - metabolism ; Theca Cells - metabolism ; Transcription Factors - deficiency ; Transcription Factors - genetics ; Transcription Factors - metabolism</subject><ispartof>Nature (London), 2011-08, Vol.476 (7358), p.101-104</ispartof><rights>Copyright Nature Publishing Group Aug 4, 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,786,790,891,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21775990$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matson, Clinton K</creatorcontrib><creatorcontrib>Murphy, Mark W</creatorcontrib><creatorcontrib>Sarver, Aaron L</creatorcontrib><creatorcontrib>Griswold, Michael D</creatorcontrib><creatorcontrib>Bardwell, Vivian J</creatorcontrib><creatorcontrib>Zarkower, David</creatorcontrib><title>DMRT1 prevents female reprogramming in the postnatal mammalian testis</title><title>Nature (London)</title><addtitle>Nature</addtitle><description>Sex in mammals is determined in the fetal gonad by the presence or absence of the Y chromosome gene Sry, which controls whether bipotential precursor cells differentiate into testicular Sertoli cells or ovarian granulosa cells. This pivotal decision in a single gonadal cell type ultimately controls sexual differentiation throughout the body. Sex determination can be viewed as a battle for primacy in the fetal gonad between a male regulatory gene network in which Sry activates Sox9 and a female network involving WNT/β-catenin signalling. In females the primary sex-determining decision is not final: loss of the FOXL2 transcription factor in adult granulosa cells can reprogram granulosa cells into Sertoli cells. Here we show that sexual fate is also surprisingly labile in the testis: loss of the DMRT1 transcription factor in mouse Sertoli cells, even in adults, activates Foxl2 and reprograms Sertoli cells into granulosa cells. In this environment, theca cells form, oestrogen is produced and germ cells appear feminized. Thus Dmrt1 is essential to maintain mammalian testis determination, and competing regulatory networks maintain gonadal sex long after the fetal choice between male and female. Dmrt1 and Foxl2 are conserved throughout vertebrates and Dmrt1-related sexual regulators are conserved throughout metazoans. Antagonism between Dmrt1 and Foxl2 for control of gonadal sex may therefore extend beyond mammals. Reprogramming due to loss of Dmrt1 also may help explain the aetiology of human syndromes linked to DMRT1, including disorders of sexual differentiation and testicular cancer.</description><subject>Aging - physiology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Cell Transdifferentiation</subject><subject>Female</subject><subject>Females</subject><subject>Feminization - genetics</subject><subject>Forkhead Box Protein L2</subject><subject>Forkhead Transcription Factors - biosynthesis</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Genes</subject><subject>Genetics</subject><subject>Granulosa Cells - cytology</subject><subject>Granulosa Cells - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Models, Biological</subject><subject>Ovary - cytology</subject><subject>Ovary - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Sertoli Cells - cytology</subject><subject>Sertoli Cells - metabolism</subject><subject>Sex Characteristics</subject><subject>Sex Determination Processes - genetics</subject><subject>Sex Determination Processes - physiology</subject><subject>Sex Differentiation - genetics</subject><subject>Sex Differentiation - physiology</subject><subject>SOX9 Transcription Factor - metabolism</subject><subject>Testis - cytology</subject><subject>Testis - metabolism</subject><subject>Theca Cells - metabolism</subject><subject>Transcription Factors - deficiency</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><issn>0028-0836</issn><issn>1476-4687</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNpVkM1LAzEUxIMotlZP3iV4X83bpMnLRRCtH1ARpJ6X7G7Sbtkvk92C_70Bq-jpwZvhN8MQcg7sChjH69YMo7fAUq4PyBSEkomQqA7JlLEUE4ZcTshJCFvG2ByUOCaTFJSaa82mZHH_8rYC2nu7s-0QqLONqS31tvfd2pumqdo1rVo6bCztuzDEMFPTJgqmrkz82zBU4ZQcOVMHe7a_M_L-sFjdPSXL18fnu9tl0oNmQ4LAADU3TiueuoKrAhCNlMppEGmu0ZWuyCUKBaVLEbTJtcO0lEII1Gj4jNx8c_sxb2xZxMre1Fnvq8b4z6wzVfZfaatNtu52GYc50xIi4HIP8N3HGLtn2270beycIXIeLRqj6eJvyi_-ZzX-BWVWb4Q</recordid><startdate>20110804</startdate><enddate>20110804</enddate><creator>Matson, Clinton K</creator><creator>Murphy, Mark W</creator><creator>Sarver, Aaron L</creator><creator>Griswold, Michael D</creator><creator>Bardwell, Vivian J</creator><creator>Zarkower, David</creator><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7ST</scope><scope>7T5</scope><scope>7TG</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PCBAR</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>R05</scope><scope>RC3</scope><scope>S0X</scope><scope>SOI</scope><scope>5PM</scope></search><sort><creationdate>20110804</creationdate><title>DMRT1 prevents female reprogramming in the postnatal mammalian testis</title><author>Matson, Clinton K ; Murphy, Mark W ; Sarver, Aaron L ; Griswold, Michael D ; Bardwell, Vivian J ; Zarkower, David</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p190t-8101893af9732fc37c188a667f9142b98fdfcb68471df2819ab9f82d6444898a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Aging - physiology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Cell Transdifferentiation</topic><topic>Female</topic><topic>Females</topic><topic>Feminization - genetics</topic><topic>Forkhead Box Protein L2</topic><topic>Forkhead Transcription Factors - biosynthesis</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Genes</topic><topic>Genetics</topic><topic>Granulosa Cells - cytology</topic><topic>Granulosa Cells - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Models, Biological</topic><topic>Ovary - cytology</topic><topic>Ovary - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Sertoli Cells - cytology</topic><topic>Sertoli Cells - metabolism</topic><topic>Sex Characteristics</topic><topic>Sex Determination Processes - genetics</topic><topic>Sex Determination Processes - physiology</topic><topic>Sex Differentiation - 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This pivotal decision in a single gonadal cell type ultimately controls sexual differentiation throughout the body. Sex determination can be viewed as a battle for primacy in the fetal gonad between a male regulatory gene network in which Sry activates Sox9 and a female network involving WNT/β-catenin signalling. In females the primary sex-determining decision is not final: loss of the FOXL2 transcription factor in adult granulosa cells can reprogram granulosa cells into Sertoli cells. Here we show that sexual fate is also surprisingly labile in the testis: loss of the DMRT1 transcription factor in mouse Sertoli cells, even in adults, activates Foxl2 and reprograms Sertoli cells into granulosa cells. In this environment, theca cells form, oestrogen is produced and germ cells appear feminized. Thus Dmrt1 is essential to maintain mammalian testis determination, and competing regulatory networks maintain gonadal sex long after the fetal choice between male and female. Dmrt1 and Foxl2 are conserved throughout vertebrates and Dmrt1-related sexual regulators are conserved throughout metazoans. Antagonism between Dmrt1 and Foxl2 for control of gonadal sex may therefore extend beyond mammals. Reprogramming due to loss of Dmrt1 also may help explain the aetiology of human syndromes linked to DMRT1, including disorders of sexual differentiation and testicular cancer.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>21775990</pmid><doi>10.1038/nature10239</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aging - physiology Animals Animals, Newborn Cell Transdifferentiation Female Females Feminization - genetics Forkhead Box Protein L2 Forkhead Transcription Factors - biosynthesis Forkhead Transcription Factors - metabolism Gene Expression Regulation Genes Genetics Granulosa Cells - cytology Granulosa Cells - metabolism Male Mice Models, Biological Ovary - cytology Ovary - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Rodents Sertoli Cells - cytology Sertoli Cells - metabolism Sex Characteristics Sex Determination Processes - genetics Sex Determination Processes - physiology Sex Differentiation - genetics Sex Differentiation - physiology SOX9 Transcription Factor - metabolism Testis - cytology Testis - metabolism Theca Cells - metabolism Transcription Factors - deficiency Transcription Factors - genetics Transcription Factors - metabolism |
| title | DMRT1 prevents female reprogramming in the postnatal mammalian testis |
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