Fiche publication
Date publication
mars 2022
Journal
Cells
Auteurs
Membres identifiés du Cancéropôle Est :
Dr MARK Manuel
Tous les auteurs :
Condrea D, Souali-Crespo S, Féret B, Klopfenstein M, Faisan S, Mark M, Ghyselinck NB, Vernet N
Lien Pubmed
Résumé
Retinoic acid signaling is indispensable for the completion of spermatogenesis. It is known that loss of retinoic acid nuclear receptor alpha (RARA) induces male sterility due to seminiferous epithelium degeneration. Initial genetic studies established that RARA acts in Sertoli cells, but a recent paper proposed that RARA is also instrumental in germ cells. In the present study, we have re-assessed the function of RARA in germ cells by genetically ablating the gene in spermatogonia and their progenies using a cell-specific conditional mutagenesis approach. We show that loss of in postnatal male germ cells does not alter the histology of the seminiferous epithelium. Furthermore, RARA-deficient germ cells differentiate normally and give rise to normal, living pups. This establishes that RARA plays no crucial role in germ cells. We also tested whether RARA is required in Sertoli cells during the fetal period or after birth. For this purpose, we deleted the gene in Sertoli cells at postnatal day 15 (PN15), i.e., after the onset of the first spermatogenic wave. To do so, we used temporally controlled cell-specific mutagenesis. By comparing the testis phenotypes generated when is lost either at PN15 or at embryonic day 13, we show that RARA exerts all of its functions in Sertoli cells not at the fetal stage but from puberty.
Mots clés
Sertoli cell, Sox9-CreERT2, Stra8-Cre, anti-RARA antibodies for IHC, mouse, retinoic acid, seminiferous epithelium, spermatogenesis, synchronization factor, tamoxifen-inducible Cre recombinase, testis
Référence
Cells. 2022 Mar 4;11(5):
