RT Journal Article
SR Electronic
T1 Meiosis Initiates In The Fetal Ovary Of Mice Lacking All Retinoic Acid Receptor Isotypes
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 716498
DO 10.1101/716498
A1 Nadège Vernet
A1 Manuel Mark
A1 Diana Condrea
A1 Betty Féret
A1 Muriel Klopfenstein
A1 Violaine Alunni
A1 Marius Teletin
A1 Norbert B. Ghyselinck
YR 2019
UL http://biorxiv.org/content/early/2019/07/26/716498.abstract
AB Gametes are generated through a specialized cell differentiation process, meiosis which, in most mammals, is initiated in ovaries during fetal life. It is widely admitted that all-trans retinoic acid (ATRA) is the molecular signal triggering meiosis initiation in mouse female germ cells, but a genetic approach in which ATRA synthesis is impaired disputes this proposal. In the present study, we investigated the contribution of endogenous ATRA to meiosis by analyzing fetuses lacking all RARs ubiquitously, obtained through a tamoxifen-inducible cre recombinase-mediated gene targeting approach. Efficient ablation of RAR-coding genes was assessed by the multiple congenital abnormalities displayed by the mutant fetuses. Unexpectedly, their germ cells robustly expressed STRA8, REC8, SYCP1 and SYCP3, showing that RAR are actually dispensable up to the zygotene stage of meiotic prophase I. Thus our study goes against the current model according to which meiosis is triggered by endogenous ATRA in the developing ovary and revives the identification of the meiosis-preventing substance synthesized by CYP26B1 in the fetal testis.