Ca2+-Induced Mitochondrial ROS Regulate the Early Embryonic Cell Cycle

Yue Han, Shoko Ishibashi, Javier Iglesias-Gonzalez, Yaoyao Chen, Nick R Love, Enrique Amaya

Research output: Contribution to journalArticlepeer-review


While it is appreciated that reactive oxygen species (ROS) can act as second messengers in both homeostastic and stress response signaling pathways, potential roles for ROS during early vertebrate development have remained largely unexplored. Here, we show that fertilization in Xenopus embryos triggers a rapid increase in ROS levels, which oscillate with each cell division. Furthermore, we show that the fertilization-induced Ca2+ wave is necessary and sufficient to induce ROS production in activated or fertilized eggs. Using chemical inhibitors, we identified mitochondria as the major source of fertilization-induced ROS production. Inhibition of mitochondrial ROS production in early embryos results in cell-cycle arrest, in part, via ROS-dependent regulation of Cdc25C activity. This study reveals a role for oscillating ROS levels in early cell cycle regulation in Xenopus embryos.

Original languageEnglish
Pages (from-to)218-231
Number of pages14
JournalCell Reports
Issue number1
Publication statusPublished - 2 Jan 2018


  • Mitochondria
  • Reactive oxygen species
  • ROS
  • mtROS
  • Xenopus
  • CDC25C
  • Cell cycle
  • fertilization
  • Ca2+ wave
  • HyPer
  • Respiratory Burst


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