Scientific Reports (Jun 2017)

Self-diploidization of human haploid parthenogenetic embryos through the Rho pathway regulates endomitosis and failed cytokinesis

  • Lizhi Leng,
  • Qi Ouyang,
  • Xiangyi Kong,
  • Fei Gong,
  • Changfu Lu,
  • Lei Zhao,
  • Yun Shi,
  • Dehua Cheng,
  • Liang Hu,
  • Guangxiu Lu,
  • Ge Lin

DOI
https://doi.org/10.1038/s41598-017-04602-y
Journal volume & issue
Vol. 7, no. 1
pp. 1 – 10

Abstract

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Abstract A diploid genome is necessary for normal mammalian development, thus haploid parthenogenetic embryos undergo frequent self-diploidization during preimplantation development; however, the underlying mechanism is unclear. In this study, time-lapse recording revealed that human haploid parthenotes (HPs) undergo self-diploidization via failed cytokinesis (FC) and endomitosis (EM). The frequencies of FC/EM were significantly higher in HPs than in normal fertilized embryos (26.3% vs. 1.6%, P 0.05). In 66.7% of the 1-cell stage HPs, furrow ingression was not observed during the time for normal cleavage, and both immunostaining and gene expression analysis of 1-cell stage HPs revealed the absence or down-regulation of several key genes of the Rho pathway, which regulates cytomitosis. Our results suggested that the major mechanism for self-diploidization is Rho pathway inhibition leading to FC/EM in the first cell cycle, and fine-tuning of this signalling pathway may help to generate stable haploid embryos for stem cell biology studies.