Fig. 6

Maternal depletion of eef1a1l2 rescues the early embryonic defects of the nanog mutant. (A) Phenotype of WT, Mnanog, Mnanog,Meef1a1l2, Mnanog,MZeef1a1l2 and Mnanog,Zeef1a1l2 embryos at 0.2, 8, 12 and 24 hpf. Scale bar: 100 μm. (B) Detection of mxtx2, mir-430 precursor, blf and sod1 in WT, Mnanog and Mnanog,Meef1a1l2 embryos by WISH at the indicated stages. Scale bar: 100 μm. (C) Proposed model of Nanog function in oogenesis and early embryogenesis of zebrafish. Top: Nanog acts as a transcriptional repressor to suppress the expression of eef1a1l2 and maintain the correct translation level of maternal mRNAs during oocyte development. Then, Nanog switches to a transcriptional activator to prime ZGA in zygotes. Bottom: In WT oocytes, Nanog inhibits the transcription of eef1a1l2 and maintains the proper level of global translation, ensuring appropriate amounts of proteins are expressed. Good egg quality and normal embryonic development is thus guaranteed. In the absence of maternal nanog (nanog^−/−), the balance of global translation is destroyed. Elevated translation results in excessive protein loading, leading to poor egg quality and failure of embryogenesis. In nanog and eef1a1l2 double-mutant oocytes (nanog^−/−,eef1a1l2^−/−), the global translation level is mitigated owing to the absence of eEF1A1l2, protein overloading is relieved and egg quality is also improved, thereby promoting a better embryonic morphology formation. Representative images shown in the schematic include data also shown in Figs 4G and 6A.