Negative Regulation of Stress-Activated MAPK Signaling in Arabidopsis

Mitogen-activated protein kinase (MAPK) cascades are an important means of signal transduction in plants and other eukaryotes, linking perception of an environmental or developmental signal to downstream targets via sequential phosphorylation of a MAPK kinase kinase, MAPK kinase, and a MAPK. The phosphorylated (activated) MAPK interacts with and alters the phosphorylation status of target proteins, including transcription factors, enzymes, and other proteins, ultimately influencing gene expression, metabolism, cell division, and growth. In Arabidopsis, MAPK cascades are known to be involved in a number of stress response signaling pathways (Colcombet and Hirt, 2008; Pitzschke et al., 2009). The regulation of dephosphorylation and inactivation of MAPKs by protein phosphatases is a critical component of MAPK signaling. A number of phosphatases have been linked to the regulation of MAPK signaling in Arabidopsis, but this aspect of MAPK signaling has not been well defined. In this issue, Bartels et al. (pages 2884–2897) report on the coordinated regulation of the MAPK MPK6 by the phosphatases MAP KINASE PHOSPHATASE1 (MKP1) and PROTEIN TYROSINE PHOSPHATASE1 (PTP1) in Arabidopsis and their relation to stress responses. Ulm et al. (2002) previously found that MKP1 interacts with several MAPKs in vitro and provided evidence that MKP1 regulates the activity level of MPK6 in planta, especially in relation to abiotic stress responses. In their work, Bartels et al. provide a detailed analysis of null mkp1 and ptp1 mutations Arabidopsis, showing that the mutations are associated with a deregulation of MPK6 that causes constitutive defense responses and leads to an accumulation of salicylic acid and camalexin and significantly reduced growth. The authors show that an mkp1 null mutation in the Columbia (Col-0) accession exhibits growth defects and constitutive defense responses, including accumulation of salicylic acid and camalexin, elevated PR gene expression, and resistance to the bacterial pathogen Pseudomonas syringae. An mkp1 ptp1 double mutant showed a more pronounced constitutive defense response than the mkp1 mutation alone (and ptp1 alone exhibited no apparent phenotype), suggesting that MKP1 and PTP1 function together to repress defense responses. Bimolecular fluorescence complementation assays confirmed that MKP1 and PTP1 interact with MPK6 in planta. Interestingly, the interaction with MKP1 was found to be primarily cytoplasmic, whereas that with PTP1 was primarily nuclear, suggesting that subcellular localization of different phosphatases may be an important component of regulation. SNC1 is a natural modifier of mkp1. snc1 partially suppresses the mkp1 ptp1 growth phenotype. Bars = 1 cm. (From Figure 5 of Bartels et al. [2009].)