Ethylene-mediated cross-talk between calcium-dependent protein kinase and MAPK signaling controls stress responses in plants

被引:246
作者
Ludwig, AA
Saitoh, H
Felix, G
Freymark, G
Miersch, O
Wasternack, C
Boller, T
Jones, JDG
Romeis, T
机构
[1] John Innes Ctr, Sainsbury Lab, Norwich NR4 7UH, Norfolk, England
[2] Max Planck Inst Plant Breeding Res, Dept Plant Microbe Interact, D-50829 Cologne, Germany
[3] Univ Basel, Inst Bot, CH-4056 Basel, Switzerland
[4] Leibniz Inst Plant Biochem, D-06120 Halle An Der Saale, Germany
关键词
D O I
10.1073/pnas.0502954102
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Plants are constantly exposed to environmental changes and need to integrate multiple external stress cues. Calcium-dependent protein kinases (CDPKs) are implicated as major primary Ca2+ sensors in plants. CDPK activation, like activation of mitogen-activated protein kinases (MAPKs), is triggered by biotic and abiotic stresses, although distinct stimulus-specific stress responses are induced. To investigate whether CDPKs are part of an underlying mechanism to guarantee response specificity, we identified CDPK-controlled signaling pathways. A truncated form of Nicotiana tabacum CDPK2 lacking its regulatory autoinhibitor and calcium-binding domains was ectopically expressed in Nicotiana benthamiana. Infiltrated leaves responded to an abiotic stress stimulus with the activation of biotic stress reactions. These responses included synthesis of reactive oxygen species, defense gene induction, and SGT1-dependent cell death. Furthermore, N-terminal CDPK2 signaling triggered enhanced levels of the phytohormones jasmonic acid, 12-oxo-phytodienoic acid, and ethylene but not salicylic acid. These responses, commonly only observed after challenge with a strong biotic stimulus, were prevented when the CDPK's intrinsic autoinhibitory peptide was coexpressed. Remarkably, elevated CDPK signaling compromised stress-induced MAPK activation, and this inhibition required ethylene synthesis and perception. These data indicate that CDPK and MAPK pathways do not function independently and that a concerted activation of both pathways controls response specificity to biotic and abiotic stress.
引用
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页码:10736 / 10741
页数:6
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