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The subcortical maternal complex modulates the cell cycle during early mammalian embryogenesis via 14-3-3

ABSTRACT: The subcortical maternal complex (SCMC) is essential for the maintenance of female fertility in mammals. Most pathogenic mutations in SCMC-encoding genes result in female reproductive failure characterized by early embryonic arrest. Assembled in oocytes, the SCMC maintains the normal cleavage of early embryos, but the mechanism regulating this function remains unclear. Here, we report that 14-3-3, a multifunctional protein, is a component of the SCMC. By resolving the cryoelectron microscopy structure of the 14-3-3-containing SCMC, we revealed that specific phosphorylation sites in TLE6 contribute to the recruitment of 14-3-3, which is indispensable for the role of the SCMC in maintaining the cleavage of mouse early embryos. Mechanistically, during the maternal-to-embryo transition, the SCMC stabilizes the 14-3-3 protein, and an acute reduction in 14-3-3 protein expression in zygotes impairs their further development to blastocysts. The SCMC containing 14-3-3 contributes to the proper control of CDC25B, thus ensuring the activation of the maturation-promoting factor and mitotic entry in mouse zygotes. Notably, we proved that the recruitment of 14-3-3 to the SCMC and the molecular link between the SCMC and CDC25B are conserved in human oocytes/embryos. This study reveals the molecular mechanism through which the SCMC regulates the cell cycle in early embryos and represents a breakthrough in fully elucidating the functions of the SCMC in mammalian early embryogenesis.

ORGANISM(S): Mus Musculus Spodoptera Frugiperda

SUBMITTER: Dong Deng

PROVIDER: PXD055498 | iProX | Tue Sep 03 00:00:00 BST 2024

REPOSITORIES: iProX

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