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Plant Cell Advance Online Publication
Published on September 29, 2009; 10.1105/tpc.109.067678

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Received April 8, 2009
Returned for revision August 28, 2009
Accepted September 8, 2009

MAP KINASE PHOSPHATASE1 and PROTEIN TYROSINE PHOSPHATASE1 Are Repressors of Salicylic Acid Synthesis and SNC1-Mediated Responses in Arabidopsis

Sebastian Bartels 1, Jeffrey C. Anderson 2, Marina A. González Besteiro 3, Alessandro Carreri 4, Heribert Hirt 5, Antony Buchala 6, Jean-Pierre Métraux 6, Scott C. Peck 2, and Roman Ulm 7*

1 Faculty of Biology, Institute of Biology II, University of Freiburg, D-79104 Freiburg, Germany
2 Department of Biochemistry, University of Missouri, Columbia, Missouri 65211
3 Faculty of Biology, Institute of Biology II, University of Freiburg, D-79104 Freiburg, Germany; Spemann Graduate School of Biology and Medicine, University of Freiburg, D-79104 Freiburg, Germany
4 Max F. Perutz Laboratories, University of Vienna, A-1030 Vienna, Austria
5 Max F. Perutz Laboratories, University of Vienna, A-1030 Vienna, Austria; Unité de Recherche en Génomique Végétale-Plant Genomics, Institut National de la Recherche Agronomique, Centre National de la Recherche Scientifique, University Evry, F-91057 Evry Cedex, France
6 Department of Biology, University of Fribourg, CH-1700 Fribourg, Switzerland
7 Faculty of Biology, Institute of Biology II, University of Freiburg, D-79104 Freiburg, Germany; Centre for Biological Signaling Studies (bioss), University of Freiburg, D-79104 Freiburg, Germany

* To whom correspondence should be addressed. E-mail: roman.ulm{at}biologie.uni-freiburg.de.

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.




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N. A. Eckardt
Negative Regulation of Stress-Activated MAPK Signaling in Arabidopsis
PLANT CELL, September 1, 2009; 21(9): 2545 - 2545.
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