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 inititate oogenesis. Meiosis is retarded in the f...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 2006-04, Vol.312 (5773), p.596-600
Main Authors: 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
Format: Article
Language:English
Subjects:
Animal reproduction
Animals
Biological and medical sciences
Cell differentiation, maturation, development, hematopoiesis
Cell physiology
Cellular biology
Cytochrome P-450 Enzyme System - genetics
Cytochrome P-450 Enzyme System - metabolism
Embryos
Enzymes
Female
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Developmental
Genes, Reporter
Germ cells
Germ Cells - physiology
Gonads
In Situ Hybridization
Lac Operon
Male
Meiosis
Mesonephros - metabolism
Mice
Mice, Knockout
Molecular and cellular biology
Naphthalenes - pharmacology
Oogenesis
Ovaries
Ovary - embryology
Ovary - metabolism
Receptors, Retinoic Acid - antagonists & inhibitors
Retinoic Acid 4-Hydroxylase
Retinoids
Reverse transcriptase polymerase chain reaction
Rodents
Sertoli cells
Sertoli Cells - enzymology
Sex Characteristics
Signal Transduction
Spermatogenesis
Testes
Testis - embryology
Testis - metabolism
Tissue Culture Techniques
Tretinoin - metabolism
Tretinoin - pharmacology
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Summary: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 inititate 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.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.1125691