Retinoid signaling determines germ cell fate in mice

Germ cells in the mouse embryo can develop as oocytes or spermatogonia, depending on molecular cues that have not been identified. We found that retinoic acid, produced by mesonephroi of both sexes, causes germ cells in the ovary to enter meiosis and initiate oogenesis. Meiosis is retarded in the fe...

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Vydané v:Science (American Association for the Advancement of Science) Ročník 312; číslo 5773; s. 596
Hlavní autori: Bowles, Josephine, Knight, Deon, Smith, Christopher, Wilhelm, Dagmar, Richman, Joy, Mamiya, Satoru, Yashiro, Kenta, Chawengsaksophak, Kallayanee, Wilson, Megan J, Rossant, Janet, Hamada, Hiroshi, Koopman, Peter
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 28.04.2006
Predmet:
Animals
Cytochrome P-450 Enzyme System - genetics
Cytochrome P-450 Enzyme System - metabolism
Female
Gene Expression Regulation, Developmental
Genes, Reporter
Germ Cells - physiology
In Situ Hybridization
Lac Operon
Male
Meiosis
Mesonephros - metabolism
Mice
Mice, Knockout
Naphthalenes - pharmacology
Oogenesis
Ovary - embryology
Ovary - metabolism
Receptors, Retinoic Acid - antagonists & inhibitors
Retinoic Acid 4-Hydroxylase
Sertoli Cells - enzymology
Sex Characteristics
Signal Transduction
Spermatogenesis
Testis - embryology
Testis - metabolism
Tissue Culture Techniques
Tretinoin - metabolism
Tretinoin - pharmacology
ISSN:1095-9203, 1095-9203
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Shrnutí:Germ cells in the mouse embryo can develop as oocytes or spermatogonia, depending on molecular cues that have not been identified. We found that retinoic acid, produced by mesonephroi of both sexes, causes germ cells in the ovary to enter meiosis and initiate oogenesis. Meiosis is retarded in the fetal testis by the action of the retinoid-degrading enzyme CYP26B1, ultimately leading to spermatogenesis. In testes of Cyp26b1-knockout mouse embryos, germ cells enter meiosis precociously, as if in a normal ovary. Thus, precise regulation of retinoid levels during fetal gonad development provides the molecular control mechanism that specifies germ cell fate.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1095-9203
1095-9203
DOI:10.1126/science.1125691