Regulation of MAPK signaling and cell death by MAPK phosphatase MKP2

Abstract

Mitogen-activated protein kinase (MAPK) pathways play crucial roles in developmental and adaptive responses. Depending on the stimulus, MAPK activation regulates a wide variety of plant cell responses, such as proliferation, differentiation and cell death, which normally require precise spatial and temporal control. In this context, protein phosphatases play important roles by regulating the duration and magnitude of MAPK activities. During infection by non-host and incompatible host microorganisms, MAPK activity can promote a local cell death mechanism called hypersensitivity response (HR), which is part of the plant defence response. HR-like responses require sustained MAPK activity and correlate with oxidative burst. We recently showed that MAPK phosphatase MKP2 positively controls biotic and abiotic stress responses in Arabidopsis. MKP2 interacts with MPK6 in HR-like responses triggered by fungal elicitors, suggesting that MKP2 protein is part of the mechanism involved in MAPK regulation during HR. Here we discuss the interplay of MAPK and MKP2 phosphatase signaling during cell death responses elicited by host-pathogen interactions.

Figure 1

Cys109 is essential for MKP2 activity in vitro. (A) SDS-polyacrylamide gel electrophoresis of GST-MKP2 (lane 1) and GST-MKP2C109S (lane 2) fusion proteins. Positions of molecular weight markers are indicated on the left. (B) Phosphatase activity of wild-type and mutant GST-MKP2 proteins. Reactions were performed using the artificial substrate OMPF and 12 mg of each fusion protein. Phosphatase activity was assayed at 30°C in 0.8 ml of reaction buffer (50 mM 3,3-dimethylglutaric acid, pH 7, 1 mM EDTA , 0.15 M NaCl, 500 µM OMPF). The amount of 3-O-methylfluorescein was measured by absorbance at 477 nm.

Figure 2

ABA/salt treatments induce MKP2 expression. Northern blot analysis of 7-day-old seedlings treated during 3 h with 100 µM ABA (A) and 250 mM NaCl (S). RAB18 expression is also shown as a positive control induced by ABA and salt treatments.

Figure 3

Hypothetical model of MKP2 function in plant HR cell death. Different mechanisms may be converging such as transcriptional (I) and post-transcriptional regulation (II), which may take place to balance and control the induction of cell-death response.