Ethylene plays a crucial role in various biological processes and therefore its biosynthesis is strictly regulated by multiple mechanisms. Posttranslational regulation, which is pivotal in controlling ethylene biosynthesis, impacts 1-aminocyclopropane 1-carboxylate synthase (ACS) protein stability via the complex interplay of specific factors. Here, we show that the Arabidopsis thaliana protein phosphatase type 2C, ABI1, a negative regulator of abscisic acid signaling, is involved in the regulation of ethylene biosynthesis under oxidative stress conditions. We found that ABI1 interacts with ACS6 and dephosphorylates its C-terminal fragment, a target of the stress-responsive mitogen-activated protein kinase, MPK6. In addition, ABI1 controls MPK6 activity directly and by this means also affects the ACS6 phosphorylation level. Consistently with this, ozone-induced ethylene production was significantly higher in an ABI1 knockout strain (abi1td) than in wild-type plants. Importantly, an increase in stress-induced ethylene production in the abi1td mutant was compensated by a higher ascorbate redox state and elevated antioxidant activities. Overall, the results of this study provide evidence that ABI1 restricts ethylene synthesis by affecting the activity of ACS6. The ABI1 contribution to stress phenotype underpins its role in the interplay between the abscisic acid (ABA) and ethylene signaling pathways.

Seeds enable plant survival in harsh environmental conditions, and via seeds, genetic information is transferred from parents to the new generation; this stage provides an opportunity for sessile plants to settle in new territories. However, seed viability decreases over long-term storage due to seed aging. For the effective conservation of gene resources, e.g., in gene banks, it is necessary to understand the causes of decreases in seed viability, not only where the aging process is initiated in seeds but also the sequence of events of this process. Mitochondria are the main source of reactive oxygen species (ROS) production, so they are more quickly and strongly exposed to oxidative damage than other organelles. The mitochondrial antioxidant system is also less active than the antioxidant systems of other organelles, thus such mitochondrial ‘defects’ can strongly affect various cell processes, including seed aging, which we discuss in this paper.