Ca2+-Induced Mitochondrial ROS Regulate the Early Embryonic Cell CycleCitation formats

  • External authors:
  • Yue Han
  • Shoko Ishibashi
  • Javier Iglesias-Gonzalez
  • Yaoyao Chen
  • Nick R Love

Standard

Ca2+-Induced Mitochondrial ROS Regulate the Early Embryonic Cell Cycle. / Han, Yue; Ishibashi, Shoko; Iglesias-Gonzalez, Javier; Chen, Yaoyao; Love, Nick R; Amaya, Enrique.

In: Cell Reports, Vol. 22, No. 1, 02.01.2018, p. 218-231.

Research output: Contribution to journalArticle

Harvard

Han, Y, Ishibashi, S, Iglesias-Gonzalez, J, Chen, Y, Love, NR & Amaya, E 2018, 'Ca2+-Induced Mitochondrial ROS Regulate the Early Embryonic Cell Cycle', Cell Reports, vol. 22, no. 1, pp. 218-231. https://doi.org/10.1016/j.celrep.2017.12.042

APA

Han, Y., Ishibashi, S., Iglesias-Gonzalez, J., Chen, Y., Love, N. R., & Amaya, E. (2018). Ca2+-Induced Mitochondrial ROS Regulate the Early Embryonic Cell Cycle. Cell Reports, 22(1), 218-231. https://doi.org/10.1016/j.celrep.2017.12.042

Vancouver

Han Y, Ishibashi S, Iglesias-Gonzalez J, Chen Y, Love NR, Amaya E. Ca2+-Induced Mitochondrial ROS Regulate the Early Embryonic Cell Cycle. Cell Reports. 2018 Jan 2;22(1):218-231. https://doi.org/10.1016/j.celrep.2017.12.042

Author

Han, Yue ; Ishibashi, Shoko ; Iglesias-Gonzalez, Javier ; Chen, Yaoyao ; Love, Nick R ; Amaya, Enrique. / Ca2+-Induced Mitochondrial ROS Regulate the Early Embryonic Cell Cycle. In: Cell Reports. 2018 ; Vol. 22, No. 1. pp. 218-231.

Bibtex

@article{f6ecd647df8a49d38ff889c74c99c40c,
title = "Ca2+-Induced Mitochondrial ROS Regulate the Early Embryonic Cell Cycle",
abstract = "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.",
keywords = "Mitochondria, Reactive oxygen species, ROS, mtROS, Xenopus, CDC25C, Cell cycle, fertilization, Ca2+ wave, HyPer, Respiratory Burst",
author = "Yue Han and Shoko Ishibashi and Javier Iglesias-Gonzalez and Yaoyao Chen and Love, {Nick R} and Enrique Amaya",
note = "Copyright {\circledC} 2017 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2018",
month = "1",
day = "2",
doi = "10.1016/j.celrep.2017.12.042",
language = "English",
volume = "22",
pages = "218--231",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Cell Press",
number = "1",

}

RIS

TY - JOUR

T1 - Ca2+-Induced Mitochondrial ROS Regulate the Early Embryonic Cell Cycle

AU - Han, Yue

AU - Ishibashi, Shoko

AU - Iglesias-Gonzalez, Javier

AU - Chen, Yaoyao

AU - Love, Nick R

AU - Amaya, Enrique

N1 - Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2018/1/2

Y1 - 2018/1/2

N2 - 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.

AB - 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.

KW - Mitochondria

KW - Reactive oxygen species

KW - ROS

KW - mtROS

KW - Xenopus

KW - CDC25C

KW - Cell cycle

KW - fertilization

KW - Ca2+ wave

KW - HyPer

KW - Respiratory Burst

U2 - 10.1016/j.celrep.2017.12.042

DO - 10.1016/j.celrep.2017.12.042

M3 - Article

C2 - 29298423

VL - 22

SP - 218

EP - 231

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 1

ER -