Zygotic genomic activation (ZGA) is a landmark event in the maternal-to-zygotic transition (MZT), and the regulation of ZGA by maternal factors remains to be elucidated. In this study, the depletion of maternal ring finger protein 114 (RNF114), a ubiquitin E3 ligase, led to 2-cell embryos developmental arrest in mice. RNF114 was proven to play a crucial role in major ZGA using immunofluorescence and transcriptome analysis. To study the underlying mechanism, we performed protein profiling in mature oocytes and found a potential substrate for RNF114, Chromobox 5 (CBX5), whose ubiquitination and degradation was regulated by RNF114. The overexpression of CBX5 prevented embryonic development and impeded major ZGA. Furthermore, TAB1 was abnormally accumulated in mutant 2-cell embryos, which was consistent with the result of in vitro knockdown of Rnf114. Knockdown of Cbx5 or Tab1 in maternal RNF114-depleted embryos partially rescued developmental arrest and the defect of major ZGA. In summary, our study reveals that maternal RNF114 plays a precise role in degrading some important substrates during MZT, the mis-regulation of which may impede the appropriate activation of major ZGA in mouse embryos.

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