We provide a transgenic approach to inactivate maternal genes in zebrafish primary oocytes. As disrupting maternal gene functions is either time-consuming or technically challenging, early developmental programs regulated by maternal factors remain mostly elusive. Maternal products are exclusive factors to drive oogenesis and early embryonic development. Our findings suggest that maternal Nanog coordinates several gene regulatory networks that shape the embryo during gastrulation. Nanog is necessary for correct spatial expression of the ventral specifying genes bmp2b, vox, and vent, and neural transcription factor her3 It is also required for the correctly timed activation of endoderm genes and for the degradation of maternal eomesa mRNA via miR-430. We further demonstrate that the cell death in MZnanog embryos is cell-autonomous. We show that three independent defects in MZnanog mutants contribute to epiboly failure: yolk microtubule organization required for epiboly is abnormal, maternal mRNA fails to degrade due to the absence of miR-430 and actin structure of the yolk syncytial layer does not form properly. Without functional Nanog, epiboly is severely affected, embryo axes do not form and massive cell death starts at the end of gastrulation. In this study we characterize the development of maternal and zygotic MZnanog null mutant zebrafish embryos. Nanog has been implicated in establishment of pluripotency in mammals and in zygotic genome activation in zebrafish.
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