During vertebrate fertilization, sperm chromatin remodeling occurs concomitantly with maternal chromosome segregation at anaphase II, leading to simultaneous formation of two pronuclei. In mammals, these processes take much longer than in other vertebrates. Here, we explore the molecular basis and physiological importance of this mammalian-specific temporal regulation using mouse oocytes. We demonstrate the involvement of protein phosphatase in temporal regulation. Early onset of pronuclear formation causes paternal-biased abnormalities in pronuclear morphology and chromosome segregation at the first mitosis. After oocyte activation, CDK1-MASTL-ENSA, a protein phosphatase 2A-suppressive pathway, remains active despite the absence of cyclin B and contributes to delayed pronuclear formation. Sustained activation of MASTL involves ribosomal S6 kinase (RSK)-mediated phosphorylation of Thr297, which is conserved only among mammalian MASTLs. Our findings reveal the role of RSK in mouse oocytes, showing that the RSK-MASTL pathway allows mammalian-specific prolonged meiotic exit and ensures the faithful conversion from sperm to paternal pronuclei.
Keywords: cell cycle; fertilization; meiotic exit; mouse early development; signaling pathway.
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