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

Yue Han, Shoko Ishibashi, Javier Iglesias-Gonzalez, Yaoyao Chen, Nick R. Love, View ORCID ProfileEnrique Amaya
doi: https://doi.org/10.1101/223123
Yue Han
1Division of Cell Matrix Biology & Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, UK
2Institute of Stem Cell and Regenerative Medicine, Medical College, Xiamen University, Xiamen, Fujian, 361102 P. R. China
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Shoko Ishibashi
1Division of Cell Matrix Biology & Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, UK
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Javier Iglesias-Gonzalez
1Division of Cell Matrix Biology & Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, UK
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Yaoyao Chen
1Division of Cell Matrix Biology & Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, UK
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Nick R. Love
1Division of Cell Matrix Biology & Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, UK
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Enrique Amaya
1Division of Cell Matrix Biology & Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, UK
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  • ORCID record for Enrique Amaya
  • For correspondence: enrique.amaya@manchester.ac.uk
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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 Ca2+ 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

  • Ca2+ 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

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted November 21, 2017.
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Ca2+-induced mitochondrial ROS regulate the early embryonic cell cycle
Yue Han, Shoko Ishibashi, Javier Iglesias-Gonzalez, Yaoyao Chen, Nick R. Love, Enrique Amaya
bioRxiv 223123; doi: https://doi.org/10.1101/223123
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Ca2+-induced mitochondrial ROS regulate the early embryonic cell cycle
Yue Han, Shoko Ishibashi, Javier Iglesias-Gonzalez, Yaoyao Chen, Nick R. Love, Enrique Amaya
bioRxiv 223123; doi: https://doi.org/10.1101/223123

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