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XB-ART-54420
Cell Rep January 1, 2018; 22 (1): 218-231.

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

Han Y , Ishibashi S , Iglesias-Gonzalez J , Chen Y , Love NR , Amaya E .


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.

PubMed ID: 29298423
PMC ID: PMC5770342
Article link: Cell Rep
Grant support: [+]
Genes referenced: ccnb2 cdc20 cdc25c cdk1 inpp5a.1 mcub psmd6 tuba4b
GO keywords: cell cycle [+]
Antibodies: Cdc25c Ab2


Article Images: [+] show captions
References:

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