Loss of Wnt4 and Foxl2 leads to female-to-male sex reversal extending to germ cells
The discovery that the SRY gene induces male sex in humans and other mammals led to speculation about a possible equivalent for female sex. However, only partial effects have been reported for candidate genes experimentally tested so far. Here we demonstrate that inactivation of two ovarian somatic...
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| Veröffentlicht in: | Human molecular genetics Jg. 16; H. 23; S. 2795 |
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| Sprache: | Englisch |
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| Abstract | The discovery that the SRY gene induces male sex in humans and other mammals led to speculation about a possible equivalent for female sex. However, only partial effects have been reported for candidate genes experimentally tested so far. Here we demonstrate that inactivation of two ovarian somatic factors, Wnt4 and Foxl2, produces testis differentiation in XX mice, resulting in the formation of testis tubules and spermatogonia. These genes are thus required to initiate or maintain all major aspects of female sex determination in mammals. The two genes are independently expressed and show complementary roles in ovary morphogenesis. In addition, forced expression of Foxl2 impairs testis tubule differentiation in XY transgenic mice, and germ cell-depleted XX mice lacking Foxl2 and harboring a Kit mutation undergo partial female-to-male sex reversal. The results are all consistent with an anti-testis role for Foxl2. The data suggest that the relative autonomy of the action of Foxl2, Wnt4 and additional ovarian factor(s) in the mouse should facilitate the dissection of their respective contributions to female sex determination. |
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| AbstractList | The discovery that the SRY gene induces male sex in humans and other mammals led to speculation about a possible equivalent for female sex. However, only partial effects have been reported for candidate genes experimentally tested so far. Here we demonstrate that inactivation of two ovarian somatic factors, Wnt4 and Foxl2, produces testis differentiation in XX mice, resulting in the formation of testis tubules and spermatogonia. These genes are thus required to initiate or maintain all major aspects of female sex determination in mammals. The two genes are independently expressed and show complementary roles in ovary morphogenesis. In addition, forced expression of Foxl2 impairs testis tubule differentiation in XY transgenic mice, and germ cell-depleted XX mice lacking Foxl2 and harboring a Kit mutation undergo partial female-to-male sex reversal. The results are all consistent with an anti-testis role for Foxl2. The data suggest that the relative autonomy of the action of Foxl2, Wnt4 and additional ovarian factor(s) in the mouse should facilitate the dissection of their respective contributions to female sex determination.The discovery that the SRY gene induces male sex in humans and other mammals led to speculation about a possible equivalent for female sex. However, only partial effects have been reported for candidate genes experimentally tested so far. Here we demonstrate that inactivation of two ovarian somatic factors, Wnt4 and Foxl2, produces testis differentiation in XX mice, resulting in the formation of testis tubules and spermatogonia. These genes are thus required to initiate or maintain all major aspects of female sex determination in mammals. The two genes are independently expressed and show complementary roles in ovary morphogenesis. In addition, forced expression of Foxl2 impairs testis tubule differentiation in XY transgenic mice, and germ cell-depleted XX mice lacking Foxl2 and harboring a Kit mutation undergo partial female-to-male sex reversal. The results are all consistent with an anti-testis role for Foxl2. The data suggest that the relative autonomy of the action of Foxl2, Wnt4 and additional ovarian factor(s) in the mouse should facilitate the dissection of their respective contributions to female sex determination. The discovery that the SRY gene induces male sex in humans and other mammals led to speculation about a possible equivalent for female sex. However, only partial effects have been reported for candidate genes experimentally tested so far. Here we demonstrate that inactivation of two ovarian somatic factors, Wnt4 and Foxl2, produces testis differentiation in XX mice, resulting in the formation of testis tubules and spermatogonia. These genes are thus required to initiate or maintain all major aspects of female sex determination in mammals. The two genes are independently expressed and show complementary roles in ovary morphogenesis. In addition, forced expression of Foxl2 impairs testis tubule differentiation in XY transgenic mice, and germ cell-depleted XX mice lacking Foxl2 and harboring a Kit mutation undergo partial female-to-male sex reversal. The results are all consistent with an anti-testis role for Foxl2. The data suggest that the relative autonomy of the action of Foxl2, Wnt4 and additional ovarian factor(s) in the mouse should facilitate the dissection of their respective contributions to female sex determination. |
| Author | Cao, Antonio Pelosi, Emanuele Nedorezov, Timur Douglass, Eric Schlessinger, David Colombino, Maria Forabosco, Antonino Ottolenghi, Chris Tran, Joseph |
| Author_xml | – sequence: 1 givenname: Chris surname: Ottolenghi fullname: Ottolenghi, Chris email: chris11@helix.nih.gov organization: Laboratory of Genetics, NIA/NIH-IRP, Baltimore, USA. chris11@helix.nih.gov – sequence: 2 givenname: Emanuele surname: Pelosi fullname: Pelosi, Emanuele – sequence: 3 givenname: Joseph surname: Tran fullname: Tran, Joseph – sequence: 4 givenname: Maria surname: Colombino fullname: Colombino, Maria – sequence: 5 givenname: Eric surname: Douglass fullname: Douglass, Eric – sequence: 6 givenname: Timur surname: Nedorezov fullname: Nedorezov, Timur – sequence: 7 givenname: Antonio surname: Cao fullname: Cao, Antonio – sequence: 8 givenname: Antonino surname: Forabosco fullname: Forabosco, Antonino – sequence: 9 givenname: David surname: Schlessinger fullname: Schlessinger, David |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17728319$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Animals, Newborn Disorders of Sex Development Female Forkhead Box Protein L2 Forkhead Transcription Factors - deficiency Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism Germ Cells - cytology Germ Cells - metabolism Humans Male Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Models, Biological Ovary - cytology Ovary - embryology Pregnancy Sex Determination Processes Sex Differentiation Testis - cytology Testis - embryology Wnt Proteins - deficiency Wnt Proteins - genetics Wnt Proteins - metabolism Wnt4 Protein |
| Title | Loss of Wnt4 and Foxl2 leads to female-to-male sex reversal extending to germ cells |
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