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10.3389/fpls.2020.560768 Front

Acknowledgements The authors thank the research resource division (RRD) (RIKEN Center for Brain Science) and RIKEN CBS-EVIDENT Open Collaboration Center (RIKEN Center for Brain Science) for technical assistance, Yukiko Nagai (RIKEN Center for Brain Science) for secretarial work, Kenichi Nagata (Nagoya University) and members of the Laboratory for Proteolytic Neuroscience (RIKEN Center for Brain Science) for beneficial suggestions

It is accepted that an excessive burden of ROS may lead to abnormal cell growth, corresponding changes in intracellular homeostasis and damage to important components of in the cell when the antioxidant defense and/or DNA repair mechanisms cannot balance the excess oxidants [29]