Ethylene-mediated cross-talk between calcium-dependent protein kinase and MAPK signaling controls stress responses in plants
Ethylene-mediated cross-talk between calcium-dependent protein kinase and MAPK signaling controls stress responses in plants
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DOI：
10.1073/pnas.0502954102
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发表时间：
2005-07-26
影响因子：
11.1
通讯作者：
Romeis, T
中科院分区：
文献类型：
--
作者：
Ludwig, AA;Saitoh, H;Romeis, T
植物不断暴露于环境变化中，需要整合多种外部胁迫信号。钙依赖性蛋白激酶（CDPKs）是植物中主要的初级钙感受器。CDPK活化，如丝裂原活化蛋白激酶（MAPK）的活化，是由生物和非生物胁迫触发，虽然不同的刺激特异性应激反应诱导。为了研究CDPK是否是保证反应特异性的潜在机制的一部分，我们鉴定了CDPK控制的信号通路。烟草CDPK 2缺乏其调节性自身抑制剂和钙结合结构域的截短形式在本氏烟草中异位表达。渗透叶响应非生物胁迫刺激与生物胁迫反应的激活。这些反应包括活性氧的合成、防御基因的诱导和SGT 1依赖的细胞死亡。此外，N-末端CDPK 2信号传导触发了植物激素茉莉酸、12-氧代-植物二烯酸和乙烯的水平提高，但没有水杨酸。这些反应，通常只观察到一个强大的生物刺激的挑战后，被阻止时，CDPK的内在自抑制肽共表达。值得注意的是，升高的CDPK信号损害了应激诱导的MAPK活化，这种抑制需要乙烯的合成和感知。这些数据表明，CDPK和MAPK途径不独立发挥作用，这两种途径的协同激活控制响应特异性生物和非生物胁迫。
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.