The degradation of maternal RNA-binding protein 4E-T regulates translational activation to ensure maternal-to-zygotic transition in mouse embryos.

CNOT1 is a potential YTHDF2 target that orchestrates maternal mRNA decay and zygotic genome activation during goat embryogenesis.

It is found that CNOT1 was upregulated during mammalian ZGA, and that its knockdown led to developmental arrest and a marked reduction in blastocyst formation, which indicates that CNOT1 is a potential YTHDF2 target that orchestrates maternal mRNA decay and ZGA during goat embryogenesis.

The RNA ac4C writer NAT10-dependent post-transcriptional regulations are prerequisites for zygotic splicing activation in mouse

It is demonstrated that the RNA ac 4 C writer NAT10 is essential for the post-transcriptional regulation of mouse zygotic splicing activation and provide valuable view for further exploration of the epigenetic mechanism during maternal-to-zygotic transition.

Pumilio and Brain tumor regulate the expression of Smaug during the Drosophila maternal-to-zygotic transition

Cyclin B3-CDK1 couples translational de-repression to embryonic mitoses via OMA protein degradation in C. elegans

During early embryogenesis, gene expression relies on maternally loaded mRNAs whose translation is controlled by RNA binding proteins. Here, we identify a critical role for the cyclin B3-CDK1 complex, known for its function in mitosis, in driving early embryonic gene expression in C. elegans. The cyclin B3-CDK1 complex works by marking the RNA binding OMA proteins (OMA-1 and OMA-2) for degradation, which ensures the de-repression and translation of their target mRNAs. OMA protein degradation relies on cyclin B3’s conserved phosphate-binding pocket, which promotes multi-site OMA phosphorylation and the generation of phospho-degrons. Notably, the phosphate-binding pocket of cyclin B3 does not substantially contribute to its mitotic roles, indicating that the mitotic and translational functions of the cyclin B3-CDK1 complex are separable. These findings establish that embryonic activation of the cyclin B3-CDK1 complex drives both mitotic divisions and mRNA de-repression, which ensures that cell division is coupled to the early gene expression program in development.

CtBP1/2 restrict DUX-dependent and independent 2C-like programs in mouse embryonic stem cells.

After fertilization, maternally deposited mRNAs are cleared, and de novo transcription is initiated through zygotic genome activation (ZGA), a core event of the maternal-to-zygotic transition in mice. 2-cell-like cells (2CLCs), a rare MERVL-positive subpopulation of mouse embryonic stem cells, partially recapitulate transcriptional features of 2-cell embryos. Although canonical MERVL-high 2CLCs depend on DUX, Dux knockout embryos can develop to term, suggesting that 2CLC models do not fully capture DUX-independent pathways associated with preimplantation transcriptional programs. Here, we show that disruption of C-terminal binding protein 1/2 (Ctbp1/2) activates both DUX-dependent minor ZGA-associated genes and DUX-independent major ZGA- and post-ZGA-associated programs. Pramel7 is derepressed independently of DUX and contributes to subsets of both programs. PRAMEL7 overexpression partially rescues transcriptional defects caused by Dux deletion and is associated with UHRF1 downregulation and DNA demethylation-linked activation of post-ZGA-associated genes. These findings identify CtBP1/2 as repressors of multiple early embryonic transcriptional programs in mouse embryonic stem cells.

SP1 controls zygotic genome activation and morula-to-blastocyst transition in mouse embryos.