Disrupted MOS signaling alters meiotic cell cycle regulation and the egg transcriptome

Loss of MOS in female mice disrupts metaphase II arrest, potentially causing infertility and germ cell tumors. Single-egg RNA sequencing revealed widespread gene expression changes in mos -/- eggs, including upregulation of cell cycle regulators like Aurka, Bub3, and Cdk7. Pathways related to RNA metabolism, transcription, and neddylation were also enriched in mos -/- eggs. Notably, the transcriptome of mos -/- eggs differed from that of chemically activated eggs. These results highlight MOS as a key regulator of the meiotic cell cycle and transcriptome integrity essential for oocyte developmental competence. Overall design: Two- to three-month-old wildtype or mos -/- C57BL/6J female mice were injected intraperitoneally with 5 I.U. of pregnant mare serum gonadotropin 48 hours before oocyte collection. All single eggs used for sequencing were collected 38-40 hours post-GV breakdown. We sequenced 29 wildtype C57BL/6J eggs, 17 chemically activated eggs, and 61 mos -/- C57BL/6J.