TY - JOUR
T1 - Retinoid signaling determines germ cell fate in mice
AU - Bowles, Josephine
AU - Knight, Deon
AU - Smith, Christopher
AU - Wilhelm, Dagmar
AU - Richman, Joy M
AU - Mamiya, Satoru
AU - Yashiro, Kenta
AU - Chawengsaksophak, Kallayanee
AU - Wilson, Megan J
AU - Rossant, Janet
AU - Hamada, Hiroshi
AU - Koopman, Peter A
PY - 2006
Y1 - 2006
N2 - 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.
AB - 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.
UR - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16574820
U2 - 10.1126/science.1125691
DO - 10.1126/science.1125691
M3 - Article
SN - 0036-8075
VL - 312
SP - 596
EP - 600
JO - Science
JF - Science
IS - 5773
ER -