Regulation of meiosis initiation in the mammalian testis: novel aspects

Abstract

Meiosis first appears at puberty in the mammalian testis, is central to spermatogenesis, and relies on androgens and retinoic acid (RA). While the role androgens play in meiosis initiation is well characterized, the mechanism behind RA action is less clear. CYP26B1 degrades RA in the fetal/prepubertal mouse testis, thus preventing meiosis occurrence before puberty, although this is not necessarily the case in humans or marsupials. CYP26B1 expression declines as Sertoli cells mature in postnatal life, but androgens are not directly involved in its downregulation. RA levels in the testis also rely on the RA-synthesizing ALDH1 enzymes. Cell-specific knockout mice for Aldh1a1/a2/a3 show that the first meiotic cycle at puberty relies on RA synthesized in Sertoli cells by ALDH1A1, while subsequent rounds use RA synthesized in meiotic germ cells by ALDH1A2. A contributive role for aldehyde oxidases in RA production has been proposed, after blocking ALDH1 action in the testis.