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>MAP KINASE PHOSPHATASE1 and PROTEIN TYROSINE PHOSPHATASE1 Are Repressors of Salicylic Acid Synthesis and SNC1-Mediated Responses in Arabidopsis
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MAP KINASE PHOSPHATASE1 and PROTEIN TYROSINE PHOSPHATASE1 Are Repressors of Salicylic Acid Synthesis and SNC1-Mediated Responses in Arabidopsis
n nnnMitogen-activated protein (MAP) kinase phosphatases are importantnegative regulators of the levels and kinetics of MAP kinaseactivation that modulate cellular responses. The dual-specificityphosphatase MAP KINASE PHOSPHATASE1 (MKP1) was previously shownto regulate MAP KINASE6 (MPK6) activation levels and abioticstress responses in Arabidopsis thaliana. Here, we report thatthe mkp1 null mutation in the Columbia (Col) accession resultsin growth defects and constitutive biotic defense responses,including elevated levels of salicylic acid, camalexin, PR geneexpression, and resistance to the bacterial pathogen Pseudomonassyringae. PROTEIN TYROSINE PHOSPHATASE1 (PTP1) also interactswith MPK6, but the ptp1 null mutant shows no aberrant growthphenotype. However, the pronounced constitutive defense responseof the mkp1 ptp1 double mutant reveals that MKP1 and PTP1 repressdefense responses in a coordinated fashion. Moreover, mutationsin MPK3 and MPK6 distinctly suppress mkp1 and mkp1 ptp1 phenotypes,indicating that MKP1 and PTP1 act as repressors of inappropriateMPK3/MPK6-dependent stress signaling. Finally, we provide evidencethat the natural modifier of mkp1 in Col is largely the diseaseresistance gene homolog SUPPRESSOR OF npr1-1, CONSTITUTIVE 1(SNC1) that is absent in the Wassilewskija accession. Our datathus indicate a major role of MKP1 and PTP1 in repressing salicylicacid biosynthesis in the autoimmune-like response caused bySNC1.展开▼
机译：ABSTRACTn n
n TOP n <字体颜色= 464c53>抽象 n 介绍 n 结果 n 讨论 n 方法 n 参考文献 n n nnn丝裂原激活蛋白（MAP）激酶磷酸酶很重要 ne调节细胞反应的MAP激酶 活化水平和动力学的调节因子。先前显示了 的双特异性 磷酸酶MAP激酶磷酸酶1（MKP1）来调节< I>拟南芥。在这里，我们报道了在生长缺陷和本构生物防御反应中， mkp1 无效突变在Columbia（Col）登录结果中 ，包括水杨酸，camalexin， PR 基因 的表达水平升高以及对细菌病原体假单胞菌 丁香油菜< / I>。蛋白质酪氨酸磷酸酶1（PTP1）也与MPK6相互作用，但 ptp1 空突变体未显示异常生长 表型。但是， mkp1 ptp1 双重突变体的明显本构防御反应 揭示了MKP1和PTP1以协调的方式抑制了 防御反应。此外，MPK3和MPK6中的突变 明显抑制 mkp1 和 mkp1 ptp1 表型， 表示MKP1和PTP1充当 MPK3 / MPK6依赖性应激信号的阻遏物。最后，我们提供证据 ，表明Col中 mkp1 的天然修饰物很大程度上是npr1-1的抗病基因 SUPPRESSOR， Wassilewskija保藏号中没有的本构词1 （ SNC1 ）。我们的数据 因此表明，MKP1和PTP1在抑制水杨酸 酸生物合成中起主要作用，所述水杨酸 SNC1引起的自身免疫样反应中。
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Faculty of Biology, Institute of Biology II, University of Freiburg, D-79104 Freiburg, Germany;
Department of Biochemistry, University of Missouri, Columbia, Missouri 65211;
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;
Max F. Perutz Laboratories, University of Vienna, A-1030 Vienna, Austria;
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;
Department of Biology, University of Fribourg, CH-1700 Fribourg, Switzerland;
Department of Biology, University of Fribourg, CH-1700 Fribourg, Switzerland;
Department of Biochemistry, University of Missouri, Columbia, Missouri 65211;
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;
