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We also found that the level of nitric oxide (NO), an important salt-responsive signaling molecule, varied in response to salt treatment depending on At Ca M1 and At Ca M4 expression.

GSNOR is considered as an important and widely utilized regulatory component of NO homeostasis in plant resistance protein signaling networks.

Here, we show that the accumulation and signaling of superoxide are mediated by three Arabidopsis proteins-RPK1, Ca M4, and Rboh F-which trigger subsequent cellular events leading to age-dependent cell death.

We demonstrate that the NADPH oxidase Rboh F is responsible for RPK1-mediated transient accumulation of superoxide, SIRK kinase induction, and cell death, all of which are positively regulated by Ca M4.

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.

This could be a conserved defensive signaling pathway in plants and animals.

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