​Sexual reproduction is crucially dependent on meiosis, a conserved, specialized cell division programme that is essential for the production of haploid gametes. Here we demonstrate that fertility and the implementation of the meiotic programme require a previously uncharacterized meiosis-specific protein, MEIOC. Meioc invalidation in mice induces early and pleiotropic meiotic defects in males and females. MEIOC prevents meiotic transcript degradation and interacts with an RNA helicase that binds numerous meiotic mRNAs.
Our results indicate that proper engagement into meiosis necessitates the specific stabilization of meiotic transcripts, a previously little-appreciated feature in mammals. Remarkably, the upregulation of MEIOC at the onset of meiosis does not require retinoic acid and STRA8 signalling.
Thus, we propose that the complete induction of the meiotic programme requires both retinoic acid-dependent and -independent mechanisms. The latter process involving post-transcriptional regulation likely represents an ancestral mechanism, given that MEIOC homologues are conserved throughout multicellular animals.​

​ Figure 1: Confocal acquisitions of representative Meioc+/+ and Meioc−/− spermatocytes stained for SYCP3 (red), MEIOC (green) and DAPI (blue). Diplo, diplotene; Lepto, leptotene; Pachy, pachytene; Prelepto, preleptotene; Zygo, zygotene. Scale bar, 5 μm.​

​ Figure 2:  Meioc+/+ and Meioc−/−  spermatocyte chromosome spreads at the indicated meiosis prophase I stages stained for SYCP1 (green) and SYCP3 (red).