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Nat Commun. 2016 Feb 19;7:10845. doi: 10.1038/ncomms10845.

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

Author information

1
Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland 4072, Australia.

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.

PMID:
26892828
PMCID:
PMC4762892
DOI:
10.1038/ncomms10845
[Indexed for MEDLINE]
Free PMC Article

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