Ca2+-induced mitochondrial ROS regulate the early embryonic cell cycle

SUMMARY While it has long been 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 oscillates with each cell division. Furthermore, we show that the fertilization induced Ca 2+ wave is both 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 for the first time, a role for oscillating ROS levels in the regulation of the early cell cycle in Xenopus embryos. Highlights ROS, including hydrogen peroxide, are produced after fertilization in Xenopus Ca 2+ signaling after fertilization induces ROS production in mitochondria Mitochondria are the major source of oscillating ROS levels ROS regulate Cdc25C activity and the early cell cycle