Mitogen-activated protein kinase phosphatase 1 controls broad spectrum disease resistance in through diverse mechanisms of immune activation.

Mitogen-activated protein Kinase Phosphatase 1 (MKP1) negatively balances production of reactive oxygen species (ROS) triggered by Microbe-Associated Molecular Patterns (MAMPs) through uncharacterized mechanisms. Accordingly, ROS production is enhanced in mutant after MAMP treatment. Moreover, plants show a constitutive activation of immune responses and enhanced disease resistance to pathogens with distinct colonization styles, like the bacterium pv. tomato DC3000, the oomycete Noco2 and the necrotrophic fungus BMM. The molecular basis of this ROS production and broad-spectrum disease resistance controlled by MKP1 have not been determined. Here, we show that the enhanced ROS production in is not due to a direct interaction of MKP1 with the NADPH oxidase RBOHD, nor is it the result of the catalytic activity of MKP1 on RBHOD phosphorylation sites targeted by BOTRYTIS INDUCED KINASE 1 (BIK1) protein, a positive regulator of RBOHD-dependent ROS production. The analysis of double mutant phenotypes suggested that MKP1 and BIK1 targets are different. Additionally, we showed that phosphorylation residues stabilizing MKP1 are essential for its functionality in immunity. To further decipher the molecular basis of disease resistance responses controlled by MKP1, we generated combinatory lines of with plants impaired in defensive pathways required for disease resistance to pathogen: double mutant defective in synthesis of tryptophan-derived metabolites, transgenic plant that does not accumulate salicylic acid, mutant impaired in abscisic acid (ABA) biosynthesis, and triple mutant impaired in proteins described as ROS sensors and that is hypersensitive to ABA. The analysis of these lines revealed that the enhanced resistance displayed by is altered in distinct mutant combinations: fully blocked resistance to , whereas displays partial susceptibility to , and , and showed compromised resistance to . These results suggest that MKP1 is a component of immune responses that does not directly interact with RBOHD but rather regulates the status of distinct defensive pathways required for disease resistance to pathogens with different lifestyles.