ALDH1A1 provides a source of meiosis-inducing retinoic acid in mouse fetal ovaries

Josephine Bowles, Chun-Wei Feng, Kim Miles, Jessica Ineson, Cassy Spiller and Peter Koopman ()
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Josephine Bowles: Institute for Molecular Bioscience, The University of Queensland
Chun-Wei Feng: Institute for Molecular Bioscience, The University of Queensland
Kim Miles: Institute for Molecular Bioscience, The University of Queensland
Jessica Ineson: Institute for Molecular Bioscience, The University of Queensland
Cassy Spiller: Institute for Molecular Bioscience, The University of Queensland
Peter Koopman: Institute for Molecular Bioscience, The University of Queensland

Nature Communications, 2016, vol. 7, issue 1, 1-8

Abstract: Abstract Substantial evidence exists that during fetal ovarian development in mammals, retinoic acid (RA) induces germ cells to express the pre-meiotic marker Stra8 and enter meiosis, and that these effects are prevented in the fetal testis by the RA-degrading P450 enzyme CYP26B1. Nonetheless, the role of RA has been disputed principally because germ cells in embryos lacking two major RA-synthesizing enzymes, ALDH1A2 and ALDH1A3, remain able to enter meiosis. Here we show that a third RA-synthesizing enzyme, ALDH1A1, is expressed in fetal ovaries, providing a likely source of RA in the absence of ALDH1A2 and ALDH1A3. In ovaries lacking ALDH1A1, the onset of germ cell meiosis is delayed. Our data resolve the conundrum posed by conflicting published data sets and reconfirm the model that meiosis is triggered by endogenous RA in the developing ovary.

Date: 2016
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DOI: 10.1038/ncomms10845

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