Proceedings of The Physiological Society

Mitochondria: Form and function (London, UK) (2017) Proc Physiol Soc 38, C01

Oral Communications

Ca2+-induced mitochondrial ROS regulate the early cell cycle in Xenopus embryos

S. Ishibashi1, Y. Han1, J. Iglesias-Gonzalez1, E. Amaya1

1. Division of Cell Matrix and Regenerative Medicine, University of Manchester, Manchester, United Kingdom.


Reactive oxygen species (ROS) act as second messengers in both homeostastic and stress response signaling pathways. The roles for ROS during early vertebrate development, however, have remained largely unknown. Using Xenopus frog embryos and a genetically encoded ROS indicator HyPer, we found that oocyte fertilization induces an increased production of ROS that is sustained during early development, with oscillations associated with each cell division. We show that fertilization induced ROS production is dependent upon Ca2+ signaling and, consistently, that Ca2+ ionophores are sufficient to induce ROS production in unfertilized oocytes. Using chemical inhibitors, we identify mitochondria as the major source of fertilization induced ROS production. Inhibiting mitochondrial ROS production causes a misregulation of Cdc25C phosphatase, resulting in cell cycle arrest during the early cleavage stages. Thus, our study reveals an important role of ROS interlinking the Ca2+ wave at fertilization and the cell cycle oscillator in Xenopus embryos.

Where applicable, experiments conform with Society ethical requirements