Maternal Nanog is critical for the zebrafish embryo architecture and for cell viability during gastrulation

Abstract

Nanog has been implicated in establishment of pluripotency in mammals and in zygotic genome activation in zebrafish. In this study we characterize the development of maternal and zygotic MZnanog null mutant zebrafish embryos. Without functional Nanog, epiboly is severely affected, embryo axes do not form and massive cell death starts at the end of gastrulation. 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. We further demonstrate that the cell death in MZnanog embryos is cell-autonomous. 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. Our findings suggest that maternal Nanog coordinates several gene regulatory networks that shape the embryo during gastrulation.