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ZFIN ID: ZDB-PUB-171204-8
Maternal Nanog is critical for the zebrafish embryo architecture and for cell viability during gastrulation
Veil, M., Schaechtle, M.A., Gao, M., Kirner, V., Buryanova, L., Grethen, R., Onichtchouk, D.
Date: 2017
Source: Development (Cambridge, England)   145(1): (Journal)
Registered Authors: Meijiang, Gao, Onichtchouk, Daria
Keywords: Epiboly, Mutant, Nanog, Transcription factor, ZGA, Zebrafish
MeSH Terms:
  • Animals
  • Bone Morphogenetic Protein 2/genetics
  • Bone Morphogenetic Protein 2/metabolism
  • Cell Survival/physiology
  • Gastrula/cytology
  • Gastrula/embryology*
  • Gastrulation/physiology*
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism
  • MicroRNAs/genetics
  • MicroRNAs/metabolism
  • Mutation
  • Nanog Homeobox Protein/genetics
  • Nanog Homeobox Protein/metabolism*
  • Repressor Proteins/genetics
  • Repressor Proteins/metabolism
  • Yolk Sac/embryology
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 29180568 Full text @ Development
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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 MZnanog (maternal and zygotic 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 owing 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 the 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.
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