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Mikedis, M. M.

Publications and source records attributed to Mikedis, M. M..

2 recordsLinked to original sources

MEIOC prevents continued mitotic cycling and promotes meiotic entry during mouse oogenesis

In multicellular organisms, germ cells transformation into haploid gametes requires that they transition from mitosis to meiosis, whereby they stop mitotic cycling and enter the meiotic cell cycle. In mammals, transcriptional activator STRA8-MEIOSIN mediates the decision to enter the meiotic cell cycle by triggering the G1-to-meiotic S phase transition. However, the molecular basis by which mammalian germ cells prevent continued mitotic cycling before entering the meiotic cell cycle remains unclear. Here, we investigate MEIOCs role in the mitosis-to-meiosis transition during mouse oogenesis by analyzing proliferation, cell cycle transcriptomics, and cell cycle-associated protein expression. MEIOC was previously shown to destabilize mRNA and repress the mitotic program after meiotic entry. Here, we demonstrate that MEIOC prevents continued mitotic cycling prior to meiotic entry in oogenic cells. We find that the mitosis-to-meiosis transition involves the repression of G1/S cyclin CCNA2 at the transcript and protein levels, and that MEIOC downregulates CCNA2 protein expression. In addition, MEIOC promotes entry into meiotic S phase by increasing Meiosin transcript abundance and consequently activating the STRA8-MEIOSIN transcription factor. Given that STRA8-MEIOSIN upregulates Meioc expression, MEIOC and STRA8-MEIOSIN form a positive feedback loop to reinforce timely meiotic initiation. We also demonstrate that BMP signaling halts mitotic cycling and promotes meiotic entry by upregulating MEIOC. We conclude that, in mouse oogenic cells, the transition from mitosis to meiosis occurs as two molecularly regulated steps- (i) halt of mitotic cycling and (ii) entry into the meiotic cell cycle - and that MEIOC modifies the cell cycle program to facilitate both steps in this transition.

developmental biology↗

Post-transcriptional repression of mRNA enhances competence to transit from mitosis to meiosis in mouse spermatogenic cells

The specialized cell cycle of meiosis transforms diploid germ cells into haploid gametes. In mammals, diploid spermatogenic cells acquire the competence to initiate meiosis in response to retinoic acid. Previous mouse studies revealed that MEIOC interacts with RNA-binding proteins YTHDC2 and RBM46 to repress mitotic genes and promote robust meiotic gene expression in spermatogenic cells that have initiated meiosis. Here, we used the enhanced resolution of scRNA-seq, and bulk RNA-seq of developmentally synchronized spermatogenesis, to define how MEIOC molecularly supports early meiosis in spermatogenic cells. We demonstrate that MEIOC mediates transcriptomic changes before meiotic initiation, earlier than previously appreciated. MEIOC, acting with YTHDC2 and RBM46, destabilizes its mRNA targets, including transcriptional repressors E2f6 and Mga, in mitotic spermatogonia. MEIOC thereby derepresses E2F6- and MGA-repressed genes, including Meiosin and other meiosis-associated genes. This confers on spermatogenic cells the molecular competence to, in response to retinoic acid, fully activate transcriptional regulator STRA8-MEIOSIN, required for the meiotic G1/S phase transition and meiotic gene expression. We conclude that in mice, mRNA decay mediated by MEIOC-YTHDC2-RBM46 enhances the competence of spermatogenic cells to initiate meiosis. SUMMARY STATEMENTRNA-binding complex MEIOC-YTHDC2-RBM46 destabilizes its mRNA targets, including transcriptional repressors. This activity facilitates the retinoic acid-dependent activation of Meiosin gene expression and transition into meiosis.

developmental biology↗