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Maternal Transcription Factor TCF12 Mediates Fertilization and Zygotic Genome Activation During Early Embryonic Development

ABSTRACT: Initial development of multicellular animals is controlled by maternal gene products stored in the oocyte. Homozygous mutations in the basic helix-loop-helix (bHLH) transcription factor TCF12 causes female infertile, but the impact of it on female reproduction is still unknown. Here, we prove evidence that TCF12 is abundantly expressed in the nucleus of growing oocytes at germinal vesicle (GV) stage, recognizing and binding target genes’ functional domain to moderate the transcriptional activity. Deletion of Tcf12 from oocytes of primordial follicles led to female sterility. Tcf12 though does not participate in meiotic maturation, unlike Tcf3 ablation, it is essential for fertilization and preimplantational development. On the one hand, Tcf12 maintains the competence of fertilization by controlling the proper expression and location of cortical granules and protease ovastacin (encoded by Astl). On the other hand, zygotes without TCF12 have a prolonged mitosis cell cycle upon a drop of protein phosphatase 2A (PP2A) activity inhibition, which further results in zygotic genome activation (ZGA) failure at the 2-cell stage. In the subsequent process of development, maternal knockout embryos gradually lose their development potential. Taken together, these observations clarified the maternal effect induced by Tcf12 ensures preimplantational development.

ORGANISM(S): Mus Musculus

SUBMITTER: Hengyu Fan

PROVIDER: PXD046728 | iProX | Tue Nov 07 00:00:00 GMT 2023

REPOSITORIES: iProX

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