Determination and Stability of Gonadal Sex

The discovery that the SRY gene induces male sex in humans and other mammals led to speculation about a possible equivalent for female sex. But females are proving to be more complicated. Several master genes appear to be autonomously involved, and female sex determination seems to remain relatively...

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Vydáno v:Journal of andrology Ročník 31; číslo 1; s. 16 - 25
Hlavní autoři: Schlessinger, David, Garcia-Ortiz, Jose-Elias, Forabosco, Antonino, Uda, Manuela, Crisponi, Laura, Pelosi, Emanuele
Médium: Journal Article Konferenční příspěvek
Jazyk:angličtina
Vydáno: Oxford, UK Am Soc Andrology 01.01.2010
Blackwell Publishing Ltd
American Society of Andrology
Témata:
Animals
Biological and medical sciences
Female
Forkhead Box Protein L2
Forkhead Transcription Factors - metabolism
Foxl2
Fundamental and applied biological sciences. Psychology
gonadal development
Gynecology. Andrology. Obstetrics
Humans
Male
Male genital diseases
Mammalian male genital system
Medical sciences
ovary
Ovary - embryology
Sex determination
Sex Determination Processes
Sex Differentiation
sex reversal
SOX9 Transcription Factor - metabolism
testis
Testis - embryology
Vertebrates: reproduction
Ovary
Reproduction
Sex determination
sex reversal
Female genital system
Development
Foxl2
gonadal development
testis
Testicle
Male genital system
ISSN:0196-3635, 1939-4640, 1939-4640
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Popis
Shrnutí:The discovery that the SRY gene induces male sex in humans and other mammals led to speculation about a possible equivalent for female sex. But females are proving to be more complicated. Several master genes appear to be autonomously involved, and female sex determination seems to remain relatively labile. Partial loss of function of the transcription factor FOXL2 leads to premature ovarian failure in women; and in animal models, Foxl2 is required for folliculogenesis as well as for maintenance, and possibly induction, of female sex determination. In the germ line, oocytes apparently form normally even in the absence of Foxl2, dependent on genes that include female‐specific factors such as Fig‐alpha, Nobox, etc. In the soma, ablation of Foxl2 or the independently expressed gene Wnt4 (likely downstream of Rspo1) can produce partial testis differentiation in XX mice, and the double knockout results in the formation of tubules and spermatogonia. This indicates that at least 2 autonomous ovarian pathways are required to antagonize testis differentiation in females, a finding that is being increasingly corroborated by studies in goats and nonmammalian vertebrates. In recent expression profiling of mouse ovaries that lack Foxl2 alone or in combination with Wnt4 or Kit/c‐Kit, we found that following Foxl2 loss, early testis genes (including the downstream effector of Sry, Sox9) and several novel ovarian genes were consistently dysregulated during embryo‐fetal development. The results support the proposal of dose‐dependent Foxl2 function and antitestis action. A partial working model for somatic development and sex determination is presented in which Sox9 is a direct antagonist of Foxl2 in the supporting cell lineage.
Bibliografie:Supported by the Intramural Research Program of the National Institute on Aging, NIH.
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ISSN:0196-3635
1939-4640
1939-4640
DOI:10.2164/jandrol.109.008201