Mitogen-activated protein (MAP) kinase phosphatases are important negative regulators of the levels and kinetics of MAP kinase activation that modulate cellular responses. The dual-specificity phosphatase MAP KINASE PHOSPHATASE1 (MKP1) was previously shown to regulate MAP KINASE6 (MPK6) activation levels and abiotic stress responses in Arabidopsis thaliana. Here, we report that the mkp1 null mutation in the Columbia (Col) accession results in growth defects and constitutive biotic defense responses, including elevated levels of salicylic acid, camalexin, PR gene expression, and resistance to the bacterial pathogen Pseudomonas syringae. PROTEIN TYROSINE PHOSPHATASE1 (PTP1) also interacts with MPK6, but the ptp1 null mutant shows no aberrant growth phenotype. However, the pronounced constitutive defense response of the mkp1 ptp1 double mutant reveals that MKP1 and PTP1 repress defense responses in a coordinated fashion. Moreover, mutations in MPK3 and MPK6 distinctly suppress mkp1 and mkp1 ptp1 phenotypes, indicating that MKP1 and PTP1 act as repressors of inappropriate MPK3/MPK6-dependent stress signaling. Finally, we provide evidence that the natural modifier of mkp1 in Col is largely the disease resistance gene homolog SUPPRESSOR OF npr1-1, CONSTITUTIVE 1 (SNC1) that is absent in the Wassilewskija accession. Our data thus indicate a major role of MKP1 and PTP1 in repressing salicylic acid biosynthesis in the autoimmune-like response caused by SNC1.

SUMMARYA primary component of plant defense is the detection of pathogen-associated molecular patterns (PAMPs) by plasma membrane-localized pathogen recognition receptors. PAMP perception results in rapid and transient activation of phosphorylation-dependent signaling pathways that lead to a wide array of defense-related responses, including extensive changes in gene expression. In Arabidopsis, several kinases, including the mitogen-activated protein kinases (MAPKs) MPK6 and MPK3, are rapidly activated after PAMP treatment, and are thought to positively regulate a wide array of defense-related responses. In contrast, negative regulation of PAMP responses by downstream phosphatases remains poorly understood. Here we report the identification of Arabidopsis MAP Kinase Phosphatase 1 (MKP1) as a negative regulator of diverse PAMP responses, including activation of MPK6 and MPK3, transient production of extracellular reactive oxygen species, accumulation of a subset of PAMP-regulated transcripts, and inhibition of seedling growth. In agreement with the enhanced PAMP response phenotypes observed in the mkp1 mutant, we found that mkp1 seedlings and adult plants are more resistant to the virulent bacterial pathogen Pseudomonas syringae pv. tomato (Pto) DC3000. Further genetic analysis revealed that MPK6, but not MPK3, is required for the mkp1-dependent increase in resistance to Pto and enhanced PAMP-induced growth inhibition observed in mkp1 seedlings. Together, our data support a role for MKP1 as a negative regulator of MPK6-mediated PAMP responses.

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SUMMARYPlants perceive UV-B radiation as an informational signal by a pathway involving UVR8 as UV-B photoreceptor, activating photomorphogenic and acclimation responses. In contrast, the response to UV-B as an environmental stress involves mitogen-activated protein kinase (MAPK) signalling cascades. Whereas the perception pathway is plant specific, the UV-B stress pathway is more broadly conserved. Knowledge of the UV-B stressactivated MAPK signalling pathway in plants is limited, and its potential interplay with the UVR8-mediated pathway has not been defined. Here, we show that loss of MAP kinase phosphatase 1 in the mutant mkp1 results in hypersensitivity to acute UV-B stress, but without impairing UV-B acclimation. The MKP1-interacting proteins MPK3 and MPK6 are activated by UV-B stress and are hyperactivated in mkp1. Moreover, mutants mpk3 and mpk6 exhibit elevated UV-B tolerance and partially suppress the UV-B hypersensitivity of mkp1. We show further that the MKP1-regulated stress-response MAPK pathway is independent of the UVR8 photoreceptor, but that MKP1 also contributes to survival under simulated sunlight. We conclude that, whereas UVR8-mediated acclimation in plants promotes UV-B-induced defence measures, MKP1-regulated stress signalling results when UV-B protection and repair are insufficient and damage occurs. The combined activity of these two mechanisms is crucial to UV-B tolerance in plants.