Journal
CELL REPORTS
Volume 21, Issue 12, Pages 3373-3380Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.11.077
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Funding
- Institute for Basic Science [IBS-R013-D1, IBS-R013-G2]
- DGIST
- National Researcher Support Program [20100020417]
- Scientific & Technological Self-Innovation Foundation of Huazhong Agricultural University [0900206305]
- Chonbuk National University
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Reactive oxygen species (ROS) are inevitable by-products of aerobic metabolic processes, causing non-specific oxidative damage and also acting as second messengers. Superoxide is a short-lived ROS that functions in various cellular responses, including aging and cell death. However, it is unclear as to how superoxide brings about age-dependent cell death and senescence. Here, we show that the accumulation and signaling of superoxide are mediated by three Arabidopsis proteins-RPK1, CaM4, and RbohF-which trigger subsequent cellular events leading to age-dependent cell death. We demonstrate that the NADPH oxidase RbohF is responsible for RPK1-mediated transient accumulation of superoxide, SIRK kinase induction, and cell death, all of which are positively regulated by CaM4. RPK1 physically interacts with and phosphorylates CaM4, which, in turn, interacts with RbohF. Overall, we demonstrate how the protein trio governs the superoxide accumulation and signaling at the cell surface to control senescence and cell death.
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